Skinfold thickness in normoglycemic offspring of patients with t2dm on graded exercise

It is uncertain if exercise can influence the occurrence of T2DM in offspring of diabetic parents. Therefore this study was designed to assess the effect of exercise on skinfold thickness of offspring of T2DM parents compared with those of non-diabetic parents. This study involved convenience sampling of 50 offspring of T2DM parents attending University College Hospital, Ibadan and 50 offspring of nondiabetic parents who were undergraduate students of the University of Ibadan, Nigeria. Participants were randomly assigned into four groups using convenience sampling method: 25 Normal-weight Offspring of Non-Diabetic Parents (NONDP), 25 Normal-weight Offspring of Diabetic Parents (NODP), 25 Overweight Offspring of Non-Diabetic Parents (OONDP) and 25 Overweight Offspring of Diabetic Parents (OODP). Each participant followed a protocol of graded exercise using the "Tummy trimmer" everyday spending 30-45 minutes daily for 24 weeks. 4 sites of skinfold thickness (supra-iliac, Biceps, Triceps and sub-scapula) were measured by skinfold caliper. Weight and Body Mass Index (BMI) were estimated using standard methods at baseline, 6 weeks, 12 weeks, 18 weeks and 24 weeks, respectively. Data were analyzed using descriptive statistic and repeated ANOVA with p-value at n less than 0.05. The results indicate that compared to baseline, there were reductions at the four sites of skinfold thickness measurements (supra-iliac, Biceps, Triceps and sub-scapular). At supra-iliac site, skinfold thickness in NONDPreductions was from 7.16 mm ± 2.02 to 6.60 mm ± 4.40. The reduction trend for supra-iliac, Biceps, triceps and subscapular skinfold sites in NONDP were 0.56 mm, 0.79 mm, 1.66 mm and 0.19 mm respectively. While the reduction trend for supra-iliac, Biceps, triceps and subscapular skinfold sites in OODP were 0.56 mm, 1.10 mm, 2.06 mm and 1.52 mm respectively. At subscapular site, the average skinfold thickness reduction trend was 0.19 mm in control group 1.53 mm in test group. Thus, graded exercise reduced skinfold thickness in all the groups. The clinical importance of this in prevention of DM among offspring of diabetic parents is quite promising

Amlodipine Corrects Changes in Blood Pressure and Baroreceptor Reflex Sensitivity in Sprague Dawley Rats Fed a High Salt Diet.

High dietary salt ingestion causes elevated blood pressure both in humans and in experimental animals.Following reports that Calcium Channel Blockers may exhibit differences in the response of blood vessels to pressor agents,this study sought to test the effects of amlodipine on blood pressure (BP) and baroreceptor reflex sensitivity (BRS) responsesto high salt ingestion. Three groups of weanling Sprague-Dawley rats i.e. control rats (CR), salt loaded rats (SR) and saltloaded rats concomitantly administered orally with amlodipine (SR+Am) were used. At the end of 6-week experimentalperiod, terminal arterial BP was determined from one femoral artery. BRS was calculated from the change in heart rate perchange in mean arterial BP following bilateral carotid artery occlusion. Plasma sodium and potassium ion concentrationswere also determined. Results show that dietary salt loading in SR significantly increased systolic and diastolic BP and Na+concentration but decreased BRS and K+ concentrations significantly. These changes were abolished in the (SR+Am) rats indicating the ability of amlodipine to ameliorate the increase in blood pressure, reduction in baroreceptor reflex sensitivityand alterations in plasma Na+ and K+ levels that were observed in SD rats fed a high salt diet.

Impaired endothelium-dependent and -independent relaxation of aorta from diabetic rats.

Vascular complication in diabetes has been reported to be due to the effects of chronic high blood glucose on the vascular system. Different relaxation mechanisms exist in the vasculature and effect of chronic high glucose on vascular relaxation mechanisms is not clearly understood. We assessed the effect of streptozotocin (STZ, 70 mg/kg, for 12 wks)-induced diabetes on vascular reactivity to isoproterenol (Isop, 10-9-10-5 M), a cAMP-dependent agent, acetylcholine (ACh, 10-9-10-5 M), a stimulant of NO (nitric oxide) synthase, sodium nitroprusside (SNP, 10-10-10-5 M), NO donor, or bradykinin (BK, 10-9-10-5 M) in the rat isolated aortic ring. Isop, ACh, SNP, or BK dose-dependently relaxed phenylephrine (PE, 10-7 M) pre-constricted ring producing a maximum relaxation of 82 % for Isop (10-5 M), 85 % for ACh (10-5 M), 100 % for SNP (10-6 M), and 30 % for BK (10-5 M) respectively. STZ attenuated Isop, ACh, and BK-induced relaxation by 45 % (n=7, pn (Fig. 5, Ref. 24).

Salt-sensitivity in normotensive and hypertensive Nigerians.

BACKGROUND: Salt-sensitivity increases the risk for the development of high blood pressure in susceptible persons and also increases the risk for cardiovascular events and mortality. OBJECTIVE: The study is to determine the pattern of salt-sensitivity among normotensive and hypertensive Nigerians. METHODS: Twenty-eight (28) hypertensive subjects (HT) and twenty-five (25) age-matched normotensive controls (NT) were given 200 mmol/day salt as sodium chloride for 5 days after control parameters had been determined. Subjects were regarded as salt-sensitive when change in mean arterial blood pressure (cMABP) between baseline levels and that after salt loading was > or = 5 mmHg. RESULTS: Systolic blood pressure and mean arterial blood pressure but not diastolic blood pressure rose significantly (p < 0.05 and p < 0.001 respectively) in NT subjects while all the parameters showed significant increases in hypertensive subjects (SBP p < 0.01; DBP p < 0.001; MABP p < 0.0001). More hypertensive subjects (60.7%) were salt-sensitive compared with normotensive (52.0%) subjects (p < 0.05). CONCLUSION: This study has demonstrated pressor responses to acute salt-loading in normotensive and hypertensive Nigerians and salt-sensitivity was higher in hypertensive subjects.

Orchidectomy attenuates impaired endothelial effects of a high-salt diet in Sprague-Dawley rats.

The effect of sex hormones on vascular reactivity is considered one of the underlying factors contributing to gender differences in cardiovascular functions and diseases. Experiments were designed to investigate the role of androgens in salt-induced hypertension by assessing the relaxation response of isolated aortic rings to acetylcholine and sodium nitroprusside in the presence or absence of l-nitroarginine methyl ester in Sprague-Dawley rats. The rats were either orchidectomized or sham-operated, with or without testosterone replacement, and were placed on a normal or high-salt diet for 6 weeks. The results indicate a significant increase (p < 0.001) in the mean arterial blood pressure of rats on the high-salt diet, when compared with control or orchidectomized rats. Orchidectomy elicited a reduction in mean arterial blood pressure (p < 0.01), while testosterone replacement normalized mean arterial blood pressure to values seen in intact rats on the high-salt diet. The high-salt diet reduced the relaxation response to acetylcholine both in the presence and absence of inhibition of endothelial nitric oxide synthase with l-nitroarginine methyl ester. Bilateral orchidectomy attenuated the impaired endothelial function induced by the high-salt diet in rats, but this was reversed by concomitant administration of testosterone, suggesting a role for androgens in enhancing long-term vascular smooth muscle tone and hence maintenance of high blood pressure in salt-induced hypertension.

Relationship between salt intake, salt-taste threshold and blood pressure in Nigerians.

BACKGROUND: Many studies have found an association between sodium intake and blood pressure. Salt taste threshold is thought to be another marker of sodium intake. OBJECTIVE: This study sought to assess two markers of sodium intake, 24-hour-urinary sodium and salt-taste threshold. We also determined the relationship between these two markers and blood pressure. METHODS: Salt taste threshold was measured by the ability of the subjects to discern the taste of salt in graded solutions of saline. Twenty-four urinary sodium was measured by flame photometry in a 24-hour urine collection. Other plasma and urine electrolytes and creatinine were measured using standard automated chemistry methods. RESULTS: There was a significantly higher salt intake measured as 24-hour urinary sodium/mmol of creatinine in the hypertensive group, (36.6±20mmol/L/mmol creatinine) compared with the normotensive group (14.8±5.8mmol/L/mmol creatinine) p<0.001. Urinary potassium was also higher in the hypertensive subjects. When the subjects were grouped into low and high salt taste threshold, the high salt threshold group also had significantly higher 24 hour urinary sodium (30.3±5mmol/L creatinine vs the low STT urinary sodium of (19.5±14 p <.05). CONCLUSION: Sodium intake measured as 24-hour urinary sodium is increased in subjects with hypertension attesting to sodium intake as a risk factor for the development of high blood pressure. Subjects with high salt taste threshold also have increased urinary sodium excretion which may predispose them to development of hypertension.

Cardiac and Kidney Weight Indices following Dietary Salt Loading and/or Chronic Nitric Oxide Synthase Inhibition in the Hooded (Aguti) Rat.

OBJECTIVES: This study was designed to investigate if dietary salt-loading and/or chronic Nitric Oxide Synthase (NOS) inhibition are associated with cardiac hypertrophy and changes in renal mass in the hooded (Aguti) rat. METHODS: Hooded rats 8-10 weeks old were divided into 4 groups viz: control, salt, L-NAME (N?-L-Arginine Methyl Ester) and salt + L-NAME. Control rats were given a normal rat diet and water. Hypertension was induced in hooded rats by giving the following treatments: rats in the salt group were given an 8% NaCl diet and water for 6 weeks; rats in the L-NAME group were fed the normal rat diet and given water containing L-NAME at a dose of 100mg/Kg/day for 4 weeks; rats in the salt + L-NAME group were given both treatments. The rats (n = 8 per group) were anaesthetized and the hearts and kidneys excised. The cardiac weight indices and the kidney weights were measured. RESULTS: The cardiac weight, cardiac weight index, left and right ventricular weight indices and kidney weight showed no significant difference in the test groups compared to control. Kidney weight/body weight (g/100g body weight) increased significantly (P<0.05) in salt+L-NAME rats (0.35 +/- 0.015) compared to control (0.31 +/- 0.013), salt-loaded (0.29 +/- 0.013) and L-NAME rats (0.20 +/- 0.010). CONCLUSIONS: Six weeks of dietary salt-loading and /or four weeks of L-NAME-loading were not associated with cardiac hypertrophy in the hooded rat. However a combination of both manoeuvres resulted in renal hypertrophy.

Artesunate causes relaxation of rat aortic rings and reduces the contractile response to noradrenaline.

OBJECTIVE: To study if the present widely used artemisin derived anti-malaria drugs have vascular effects. METHODS: Aortic rings were obtained from adult male Sprague-Dawley rats. The rings were mounted in an organ bath and tension recorded using isometric force transducers. After pre-contraction with noradrenaline, cumulative doses of artesunate were added to the bath containing the rings. The effects of nitric oxide inhibition with L-NAME, on the responses to artesunate were also assessed. Lastly the effects on the contractile responses of the rings to noradrenaline (NA) were determined before and after incubation in artesunate. RESULTS: Cumulative addition of artesunate from 6 x 10(-4) to 6 x 10(-1) mg/ml resulted in relaxation of pre-contracted aortic rings. L-NAME significantly reduced the relaxation response to artesunate (P < 0.05). Vascular contraction response to NA was significantly reduced (P < 0.01) following the addition of artesunate. CONCLUSION: Artesunate causes relaxation of precontracted rat aortic rings which is partly mediated by Nitric Oxide (EDRF). It also reduces the contractile responses of the rings to noradrenaline.

Effect of chloroquine on strips of non-pregnant and pregnant mice uteri in-vitro.

Chloroquine (CQ) remains the household drug for the treatment of malaria especially among pregnant women. However, there are reports that CQ inhibits the contractile process in non-pregnant rat's uterus. The aim of this study is to compare responses to CQ between non-pregnant and pregnant mice and identify some mechanisms involved. Experiments were carried out in non-pregnant and pregnant mice pretreated 24 hours before with 1.5 mg/kg-body weight stilboesterol given orally. Strips of uterine smooth muscle, approximately 5 mm in diameter, were mounted in a 20 ml organ bath containing De Jalon solution bubbled with a 95% O2-5% CO2 gas mixture. Responses of the strips to graded concentration of acetylcholine (ACh) (10(-9) to 10(-5) mol/L), oxytocin (OXY) (10(-5) to 10(-2) IU/ml) and CQ (10(-6) to 4 x 10(-4) mol/L) were investigated. The strips were then incubated in 4 x 10(-4) mol/L CQ for 15 mins and the cumulative dose responses for OXY were repeated. To investigate mechanism of action, the strips were incubated for 15 mins in N(w)-nitro L-arginine methyl ester (L-NAME) and the cumulative responses to CQ repeated. Each investigation was carried out in fresh tissue mounted on Grass Model FT03 force transducer coupled unto a 4-channel Grass Model 7D Polygraph. CQ (low to moderate level), ACh and OXY led to increases in contractile responses in the uteri. There were greater contractile responses in non-pregnant than pregnant mice to CQ and ACh. At high doses, CQ had an inhibitory effect on the uterine contraction. Incubating in CQ led to abolition of contractile responses to OXY and ACh. In the presence of L-NAME, inhibitory effect of CQ at high doses was attenuated in pregnant mice only. The results suggest that CQ at high doses inhibits contractile responses in non-pregnant and pregnant mice. Enhanced nitric oxide bioactivity attenuated this inhibitory effect.

Role of nitric oxide in salt and water excretion in experimental hypertension in hooded (Aguti) rats.

OBJECTIVES: The present study was designed to investigate the suitability of the hooded rat in experimental hypertension studies and to investigate some mechanisms underlying the development of hypertension. METHODS: Hooded rats were randomly divided into 4 groups: control, Salt, L-NAME (N' -Nitro-L-Arginine Methyl Ester) and salt+L-NAME. Control rats received a normal rat chow. Hypertension was induced in the test groups by giving 8% salt and/or 100mg/kg/day L-NAME for 6 and/or 4 weeks respectively. Urine and serum samples were collected from the rats and analysed for their cation contents. The blood pressure of the rats was measured. RESULTS: The mean arterial pressure (mean +/- SEM; mm Hg) increased significantly in the test groups of rats (salt: 138.3+/-4.0; L-NAME: 165.7+/-6.0; salt+L-NAME: 133.35.2) when compared with control (88.42.7; P<0.05). Water consumption, urine volume and Na+ excretion increased significantly in salt-loaded and salt+L-NAME groups compared with control (P<0.05) but remained similar in L-NAME rats. These values were however significantly less in salt+L-NAME rats compared with salt loaded rats (P<0.05). Urinary K+ excretion, serum Na+ and K+ concentrations remained similar in all groups. CONCLUSIONS: These results suggest that the hooded rat may be useful for experimental hypertension studies. Attenuation of the diuretic and natriuretic responses to salt loading in the presence of L-NAME suggests that nitric oxide is involved in the mechanisms involved in these responses. It is concluded that nitric oxide deficiency may exacerbate salt and volume retention in salt-loaded rats and possibly play a role in the subtle renal defect underlying salt sensitive hypertension.

Vasodilator effects of leptin on canine isolated mesenteric arteries and veins.

1. Although leptin increases sympathetic nerve activity and blood pressure, its direct action on large arterial rings is to cause relaxation. However, it is the small resistance arteries and veins that are important in blood pressure control. The effects of leptin on these small vessels has not been reported previously in the canine and the effect of leptin on the capacitance vessels is not known. 2. In the present study, third- or fourth-order canine mesenteric arteries and veins were isolated and placed in a perfusion myograph and preconstricted with noradrenaline. The responses to graded concentrations of leptin were determined and the role of nitric oxide was assessed by administration of N(G)-nitro-l-arginine methyl ester (l-NAME), a blocker of nitric oxide synthase. 3. Leptin induced dose-related dilatations in both arterial and venous segments. The mean (+/-SEM) maximum increases in the diameter of the arteries and veins were 25.0 +/- 4.8 and 29.9 +/- 2.0% of the initial preconstriction, respectively. Relaxations of both arteries and veins were abolished by l-NAME or by endothelium denudation, although dilatations were still obtained to sodium nitroprusside, a nitric oxide donor. 4. These results indicate that leptin dilates canine small mesenteric arteries and veins by a mechanism involving endothelial release of nitric oxide. This observation may result in a decrease of peripheral resistance and venous return and, hence, counteract the leptin-induced neurally mediated vasoconstriction that has been reported previously.

Morinda lucida reduces contractility of isolated uterine smooth muscle of pregnant and non-pregnant mice.

The present work investigated the effect of Morinda lucida (M. lucida) extract on isolated uterine smooth muscle of pregnant and non-pregnant mice. Pregnant and non-pregnant mice were pretreated with oral stilboesterol (0.1 mg/kg body weight) and killed by cervical dislocation. Thin strips of the uterus were cut and mounted in a 20 ml organ bath containing De Jalon solution bubbled with 95%O2-5% CO2 gas mixture. The strips were connected to a force transducer coupled to a Grass 7D Polygraph for the recording of isometric tension. Effects of graded concentrations of oxytocin (OXY; 10-5-10-2 mol/L), acetylcholine (ACh; 10-9-10-5 mol/L) and M. lucida extract (0.015-1.5 mg/ml) were recorded. Fresh uterine strips were then incubated with M. lucida extract for 5 mins and cumulative response to OXY was repeated. Another set of fresh strips was incubated in L-NAME for 15 mins and the cumulative responses to M.lucida extract were repeated. OXY resulted in increased contractile responses in both pregnant and non-pregnant uterine muscles. M. lucida resulted in relaxation of the uterine smooth muscle in both pregnant and non-pregnant mice at all doses. However, at 1.5mg/ml, M. lucida completely blocked spontaneous uterine contractions. Following incubation with L-NAME, M. lucida extract led to a slightly greater relaxation of the uterine strips. In conclusion, M. lucida reduced contractility of uterine smooth muscle in both pregnant and non-pregnant mice as well as blocking contractile responses to OXY and Ach in uterine smooth muscle of pregnant and non-pregnant mice. There was no significant alteration of M. lucida activity by L-NAME suggesting that the action of the compound on uterine muscle is not associated with impaired nitric oxide synthase.

Endothelum-dependent and-independent relaxations in aortic rings obtained from hypertensive hooded (Aguti) rats.

Experimental hypertension studies are few in the hooded (Aguti) rat. The present study was designed to investigate the usefulness of this rat strain for experimental hypertension studies and to test the hypothesis that the hypertension may be associated with a diminution of endothelium dependent and independent relaxations. Hypertension was induced in inbred hooded rats (n=8 each) by administering 8% salt in the diet and /or 100 mg/kg/day Nomega-nitro-L-arginine-methyl-ester (L-NAME) in the drinking water for six and/or four weeks respectively. The rats were anaesthetized using a 25% urethane and 1% chloralose mixture given intraperitoneally at a dose of 5 mg/kg. Their blood pressure was measured invasively. Thereafter, relaxations of rat aortic preparations to acetylcholine, histamine and sodium nitroprusside (SNP) were assessed using standard organ bath conditions. Probability level of 0.05 was taken as statistically significant. The mean arterial pressure (MAP;mm Hg) rose significantly in all test groups (Salt: 148.3 +/- 4.6; L-NAME: 181.7 +/-8.3; Salt+L-NAME:154.9 +/-8.7) compared with control (94.2 +/-6.8; [P < 0.05]. The MAP was significantly [P < 0.05] higher in the L-NAME group than in all the other groups. The heart rate fell significantly in the salt + L-NAME group compared to control [P <0.05].The IC50 of acetylcholine in aortic rings from L-NAME rats (7.9 x 10(-1) +/- 6.0 x 10(-3)) was significantly higher than in rings from control (9.4 x 10(-8) +/- 2.8 x 10(-8)), salt (7.8 x 10(-7) +/- 4.7 x 10(-7)) and salt + L-NAME (3.3 x 10 (-7) +/- 2.1 x 10(-7)) rats [P < 0.05]. The IC50 of histamine and SNP in the rings from the test groups of rats showed no significant difference from control. Also, endothelium dependent and independent relaxations were preserved in the various forms of hypertension studied except in chronic NOS inhibition where the former was attenuated in response to acetylcholine.

Carotid chemoreceptor reflexes following dietary salt loading in rats.

There is a strong association between salt intake and hypertension. Alterations in baroreceptor activity, which precede and contribute to the elevation in blood pressure, have also been shown to affect chemoreceptor reflex response. Dietary salt loading with 8% sodium chloride was carried out in Sprague Dawley rats aged 8 weeks for a period of 5-6 weeks. Blood pressure was thereafter recorded under anaesthesia from the common carotid artery with a Grass Polygraph 7D model, whereas serum Na and K concentrations were measured using a flame photometer. Salt loading resulted in elevated arterial blood pressure as well as hypokalaemia. Stimulation of the carotid chemoreceptor by injection of sodium dithionite resulted in elevated arterial blood pressure, decreased heart rate and hyperventilation in both control and salt-loaded rats. However, the bradycardic response as estimated by the difference in percentage reduction in heart rate was significantly higher in salt rats (36%) than in the control rats (10%). The results indicate that a high-salt diet results in enhanced bradycardic response to carotid chemoreceptor stimulation and that this observation may be related to the attendant hypokalaemia.

Role of the endothelium in the vascular effects of vitamin C in rats.

The present study was undertaken to determine whether vascular responsiveness and endothelial function were altered in rats after 8 weeks of vitamin C treatment. Thoracic aortae were isolated from control and vitamin C-treated rats and analysed for changes in vascular reactivity. Vitamin C treatment attenuated the contractile response of aortic rings to noradrenaline and KCl. Removal of the endothelium increased the sensitivity of control rings but did not alter the effect of vitamin C. Endothelium-dependent relaxation to acetylcholine was significantly (P<0.05) enhanced by vitamin C, but the endothelium-independent relaxation response to sodium nitroprusside was not affected by vitamin C. The results suggest that the endothelium is not involved in the reduction in vascular sensitivity to contractile agonists caused by vitamin C. In addition, the enhancement of endothelium-dependent relaxation may be due to protection of nitric oxide against inactivation by oxygen free radicals.

The effects of nifedipine and thapsigargin on the responses of pressurized rat mesenteric artery to 5-hydroxytryptamine and norepinephrine.

The responses of isolated pressurized second order mesenteric resistance arteries of Wistar rats, superfused with physiological salt solution (PSS) were determined to 5-hydroxytryptamine (5-HT) and norepinephrine (NE). The contractility of the vessel was enhanced in response to 5-HT compared to NE (P<.001, ANOVA). The L-type calcium ion channel blocker, nifedipine (10(-6) M) abolished the response to either 5-HT or NE. In vessels with intact endothelium, thapsigargin (TG, 10(-6) M), which inhibits uptake of calcium ions into intracellular stores, significantly reduced the contractile response to 5-HT (P<.02) but had little or no effect on the response to NE (P=.2). However, in vessels denuded of the endothelium, there was no significant difference in the response of the mesenteric artery, after TG, to either 5-HT or NE. The results indicate that, in the rat mesenteric resistance vessel, both 5-HT and NE use calcium ions from extracellular sources for contraction, while NE relies mainly on extracellular ion influx with little or no contribution from intracellular sources. The reduced response of the de-endothelized vessel to 5-HT after TG suggests that the utilization of intracellular stores by this agonist is endothelium-dependent. These observations may explain the enhanced responsiveness of the mesenteric artery to 5-HT when compared with NE.

Change in endothelial function in mesenteric arteries of Sprague-Dawley rats fed a high salt diet.

A high salt diet in some species results in elevated arterial blood pressure and alterations in vascular smooth muscle responses to agonists. Weanling male Sprague-Dawley rats were given either a high salt diet containing 8 % or a low salt diet of 0.4 % sodium chloride for a period of 4 weeks. At the end of the feeding period, tail systolic pressure was higher in the high salt than in low salt rats. The rats were then killed and the intestines removed. Vascular smooth muscle (VSM) responses were estimated from the changes in lumenal diameter of pressurised second order mesenteric resistance arteries. High salt diet resulted in enhanced VSM responses to noradrenaline. The vessels dilated in response both to acetylcholine and to sodium nitroprusside and the responses were similar in vessels from both high and low salt rats. However, vessels from high salt rats were resistant to the blocking of endothelium derived nitric oxide (EDNO) with L-NAME and the responses were instead abolished by blocking endothelium derived hyperpolarising factor (EDHF) with apamin and charybdotoxin. These results show that in Sprague-Dawley rats, a high salt diet enhances the vasoconstriction in response to noradrenaline. The vasodilatory responses to acetylcholine were not significantly changed. However, they appeared to be mediated mainly by EDHF rather than by EDNO as in the low salt animals.

Effect of dietary salt loading and high-calcium diet on vascular smooth muscle responses and endothelium function in rats.

1. The present study examined the effects of concurrent manipulation of dietary calcium and salt on contractile responses of vascular smooth muscle (VSM) and endothelial function of aortic rings from Sprague-Dawley rats. 2. Salt loading enhanced the contractile response of the aortic rings to noradrenaline (NA), an effect that was blunted by a high calcium intake. 3. Removal of the endothelium and incubation of aortic rings in physiological salt solution containing methylene blue increased the sensitivity of the rings to NA. 4. The increase in the sensitivity of aortic rings induced by endothelium removal was more pronounced in aortic rings from salt-loaded rats. 5. Acetylcholine caused similar degrees of relaxation in all experimental groups, but the relaxation to histamine was smaller (P < 0.05) in salt-loaded rats than in other groups of rats; however, after removal of the endothelium, the contractile response to histamine was higher in salt-loaded rats. 6. The results indicate that the hypersensitivity of isolated aortic rings to agonists, as observed in salt-loaded rats, is due to altered responses of the VSM and not as a result of changes in the endothelium. In addition, salt loading tends to increase the synthesis of endothelium-dependent relaxing factor. The ability of salt loading to enhance the contractile responses of VSM to agonists can be prevented by supplementing the diet with high calcium.

Differential responses of rat aorta and mesenteric artery to norepinephrine and serotonin in vitro.

The differences in the responses of isolated ring segments of aorta and mesenteric artery of rat have been investigated. The aortic rings showed higher sensitivity to norepinephrine than the mesenteric artery rings. On the other hand, the sensitivity of the mesenteric artery to serotonin was 17 times greater than that of the aortic ring segments. However, there was no difference between the sensitivity of the aorta and the mesenteric artery to potassium chloride stimulation. There was also no difference in the contractile responses of the aorta and the mesenteric artery to calcium chloride either during norepinephrine stimulation or during stimulation with serotonin. The phasic contraction of the aorta to norepinephrine was greater than the phasic contraction of the mesenteric artery to this agonist while the magnitude of phasic contraction of the aorta to serotonin was lower than that of the mesenteric artery. These results suggest that the differences in the contractile responses of the rat aorta and the mesenteric artery to norepinephrine and serotonin are dependent on the ability of these agonists to mobilise calcium from intracellular stores.

High dietary calcium attenuates the enhanced vasoconstrictor effects of serum from salt-loaded rats.

The effect of calcium supplementation and salt loading on blood pressure, serum electrolytes, and vasoconstrictor response to serum and vascular prostaglandin synthesis were studied in Sprague Dawley rats. The mean arterial pressure of salt-loaded rats was higher (P < 0.05) than the mean arterial pressure of normal rats, salt-loaded-calcium-fed rats, or calcium-fed rats. Serum from salt-loaded rats had lower serum potassium (4.47 +/- 0.39 Meq/L) and salt-loaded-calcium-fed rats (5.14 +/- 0.47 Meq/L). The vasoactivity of serum from the salt-loaded rats (1116.67 +/- 160.13 mg) was higher than the contraction produced by sera from normal rats (643.80 +/- 37.50 mg) or from salt-loaded-calcium fed rats (562.47 +/- 37.50 mg). Indomethacin did not alter the contractile response of aortae from normal rats and salt-loaded rats to noradrenaline, but it significantly enhanced the contractile response of aortae from salt-loaded-calcium-fed and calcium-fed rats. The results suggest that dietary calcium may lower blood pressure by reducing the circulating levels of some plasma vasoactive factors induced by salt loading and by enhancing the synthesis of vasodilator prostaglandins.