Effect of PaCO2 and PaO2 on lidocaine and articaine toxicity.

Alterations in arterial PaCO2 can influence local anesthetic toxicity. The objective of this study was to evaluate the effect of stress-induced changes in PaCO2 and PaO2 on the seizure threshold of lidocaine and articaine. Lidocaine (2% with 1 : 100,000 epinephrine) or articaine (4% with 1 : 100,000 epinephrine) was administered intravenously under rest or stress conditions to 36 rats separated into 4 groups. Propranolol and prazosin were administered preoperatively to minimize cardiovascular effects of epinephrine. Mean arterial pressure (MAP), heart rate (HR), and arterial pH, PaCO2, and PaO2 were measured. Results showed no differences in MAP, HR, or pH. Stress significantly increased the latency period for the first tonic-clonic seizure induced by a toxic dose of both lidocaine and articaine (P < .05). Seizures were brought on more rapidly by articaine. No significant difference between toxic doses of lidocaine and articaine was noted. Stress raised the seizure threshold dose for both drugs and significantly (P < .01) increased arterial PaO2 from 94.0 ± 1.90 mm Hg to 113.0 ± 2.20 mm Hg, and reduced PaCO2 from 36.0 ± 0.77 mm Hg to 27.0 ± 0.98 mm Hg. In conclusion, reduction in PaCO2 and/or increase in PaO2 raised the seizure threshold of lidocaine and articaine. This study also confirmed that lidocaine and articaine have equipotent central nervous system toxicity.

Use of sugar cane to feed lactating dairy goats / [Uso da cana-de-açúcar na alimentação de cabras leiteiras em lactação]

The aim of the present study was to assess the effects of replacing corn silage with sugarcane in the diet of lactating Saanen goats and to determine their intake and digestibility of nutrients, ingestive behavior, milk yield and composition. The experimental diets were composed of increasing levels (0, 33, 66 and 100%) of substitution in dry matter (DM). Twelve multiparous Saanen goats, with an average body weight of 45.2kg, average milk yield of 3.0kg day-1, distributed in a triple latin square experimental design (4 × 4) were used. The dry matter intake (DMI) and other nutrients were estimated through the difference between the total nutrient in the food offered and its total in the leftovers. The DMI, crude protein, neutral detergent fiber (NDF) and total digestible nutrients were not influenced, but the apparent digestibility of DM and NDF decreased. Feeding time and feeding efficiency were not influenced, the rumination and total chewing times increased, and the leisure time decreased, both linearly. Milk yield was not influenced by substitution levels, but corrected milk yield to 3.5% fat decreased. Sugar cane represents a dietary alternative for goats with medium milk yield in critical periods of forage, since it does not change the consumption of DM and milk yield, even with the apparent declining digestibility of some nutrients, influencing the ingestive behavior of the animals.(AU)

O objetivo do presente estudo foi avaliar os efeitos da substituição da silagem de milho por cana-de-açúcar na dieta de cabras Saanen em lactação e determinar a ingestão e a digestibilidade de nutrientes, o comportamento ingestivo, a produção e a composição do leite. As dietas experimentais foram compostas de níveis crescentes (0, 33, 66 e 100%) de substituição na matéria seca (MS). Doze cabras Saanen multíparas, com peso corporal médio de 45,2kg, produção média de leite de 3,0kg dia-1, foram distribuídas em delineamento experimental triplo quadrado latino (4 × 4). A ingestão de matéria seca (IMS) e de outros nutrientes foi estimada por meio da diferença entre o total de nutrientes nos alimentos oferecidos e o total nas sobras. A IMS, a proteína bruta, a fibra em detergente neutro (FDN) e os nutrientes digestíveis totais não foram influenciados, mas a digestibilidade aparente da MS e da FDN diminuiu. A produção de leite não foi influenciada pelos níveis de substituição, mas a produção de leite corrigida para 3,5% de gordura diminuiu. A cana-de-açúcar representa uma alternativa alimentar para cabras com produção média de leite em períodos críticos de forragem, pois não altera o consumo de MS e a produção de leite, mesmo diminuindo a digestibilidade aparente de alguns nutrientes e influenciando o comportamento ingestivo dos animais.(AU)

Sex hormone modulation of ventricular hypertrophy in sinoaortic denervated rats.

The influence of sex hormones on the development of left ventricular hypertrophy was investigated in baroreceptor-denervated rats. A significant increase (p less than 0.01) in the left ventricular weight/body weight ratio was observed in male but not in female rats 15 days after operation, compared to age- and sex-matched sham-operated rats. This differential hypertrophy occurred despite the development of a significant elevation in arterial blood pressure in both sexes. Castration prior to sinoaortic denervation did not change the level of arterial hypertension but caused a significant reduction (p less than 0.01) in left ventricular weight in male rats and a significant increase (p less than 0.01) in female rats. The pretreatment of male and female sinoaortic denervated and castrated rats with testosterone resulted in ventricular hypertrophy similar to that observed in intact male sinoaortic denervated rats. Pretreatment with estradiol, however, suppressed the left ventricular hypertrophy in intact male rats but did not change the normal ventricular mass observed in intact female sinoaortic denervated rats. These results indicate that the development of left ventricular hypertrophy in sinoaortic denervated rats is modulated by sex hormones, and that testosterone exerts a facilitatory and estradiol an inhibitory action.

Time course of changes in sigmoidal-fitting baroreceptor curves in one-kidney, one clip hypertensive rats.

The present study examined the time course of changes in baroreceptor reflex function by means of sigmoidal curve-fitting analysis in conscious, unrestrained renovascular one-kidney, one clip (1K1C) rats at 1, 3, 7, 15, 30, and 60 days after renal artery clipping. The reflex heart rate responses were elicited by alternate intravenous bolus injections of phenylephrine (change, +5 to +50 mm Hg) and sodium nitroprusside (change, -5 to -50 mmHg). Atropine methylnitrate and atenolol were given to evaluate the responses mediated by the cardiac sympathetic or vagal component, respectively. The average baroreceptor reflex gain (sensitivity) decreased progressively (day 1, 3.35 +/- 0.3 beats per minute [bpm] per millimeter of mercury), reaching a maximal attenuation in the 30-day 1K1C group (1.83 +/- 0.5 bpm/mm Hg) compared with sham rats (approximately 4.60 bpm/mm Hg). The data showed a decreased vagal activity contributing to the attenuation of the baroreceptor gain only in the 30-day 1K1C group. In contrast, the cardiac sympathetic component of the baroreceptor reflex was significantly decreased in all 1K1C groups (from 2.10 +/- 0.4 to 0.50 +/- 0.2 bpm/mm Hg) compared with the respective sham groups (from 3.80 +/- 0.3 to 3.10 +/- 0.4 bpm/mm Hg). These results suggest that a reduced contribution of the sympathetic component to the baroreceptor heart rate reflex may be the main cause of the progressive attenuation of the baroreceptor reflex sensitivity observed in conscious 1K1C hypertensive rats.

Endothelium-dependent and endothelium-independent effects of adenosine diphosphate in renovascular hypertension.

Norepinephrine-induced responses in isolated perfused mesenteric vascular bed from normotensive and renovascular hypertensive rats were examined in the presence of adenosine diphosphate (ADP, 2 x 10(-6) M). Responses to norepinephrine were significantly greater in vessels from hypertensive rats. Norepinephrine-induced contractions increased after the removal of endothelium. N omega-Nitro-L-arginine (L-NOARG), a potent inhibitor of nitric oxide formation, similarly increased contractions. The greatest responses were obtained, however, after treatment of the vascular segments with methylene blue. The presence of ADP caused significant endothelium-dependent decreases in contractions. Although decreases caused by ADP in vessels with endothelium after treatment with L-NOARG were not statistically significant, a tendency to decreased responses seems to suggest that L-NOARG diminishes but does not completely prevent the effect of ADP in mesenteric vessels. Methylene blue partially reduced the endothelium-dependent ADP-induced relaxant effects in sham-operated nephrectomized rats. A tendency to increased contractions to norepinephrine was observed in the presence of ADP after removal of endothelium. Thus, in the mesenteric resistance arteries of the rat under stimulation by ADP, it appears that nitric oxide released from L-arginine and the activity of soluble guanylate cyclase account only in part for the endothelium-dependent decreased responses to norepinephrine. When nitric oxide formation or soluble guanylate cyclase activity are depressed simultaneously with endothelium damage, ADP released from platelets or red blood cells may be an important factor that acts synergically with vasoconstrictor stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)

L-arginine restores the effect of ouabain on baroreceptor activity and prevents hypertension.

In spontaneously hypertensive rats, ouabain exerts an excitatory effect on baroreceptor nerve activity (BNA). The aim of this study was to determine the effects of ouabain on BNA in other experimental models of hypertension and its interaction with nitric oxide. Rats were made hypertensive using the procedures for N(omega)-nitro-L-arginine methyl ester (L-NAME), deoxycorticosterone acetate (DOCA) salt, and 2-kidney, 1 clip (2K1C) hypertension models. In these groups, systolic arterial pressure was 195+/-7, 149+/-6, and 148+/-4 mm Hg, respectively, compared with 110+/-4 mm Hg in normotensive rats. Acute ouabain administration had an excitatory effect on BNA in normotensive rats (37+/-4%), an inhibitory effect in L-NAME hypertensive rats (-60+/-7%), and no effect in DOCA-salt and 2K1C hypertensive rats. The effects of ouabain were not related to arterial pressure levels, and no excitatory effect on BNA was observed in prehypertensive DOCA-salt rats. Long-term administration of L-arginine (3 g x kg(-1) x day(-1)) prevented DOCA-salt (121+/-8 mm Hg) and 2K1C (104+/-4 mm Hg) hypertension, markedly attenuated L-NAME (130+/-9 mm Hg) hypertension, and restored the excitatory effect of ouabain on BNA in these groups to levels similar to the normotensive rats and their respective control groups. We conclude that ouabain has a diverse effect on BNA in experimental models of hypertension, and it can be normalized by L-arginine. The data also indicate that nitric oxide may play a pivotal role in mediating the excitatory effect of ouabain on BNA, and we speculate that a therapeutic combination of ouabain and L-arginine may be beneficial in secondary hypertension.

Effects of chlorthalidone on ventricular hypertrophy in deoxycorticosterone acetate-salt hypertensive rats.

Diuretics have been the mainstay of long-term treatment of hypertension, but there is no evidence suggesting that diuretics may be effective in reducing cardiac hypertrophy associated with hypertension. Thus, the present study was carried out to elucidate if long-term treatment with chlorthalidone (8 mg per animal per day added to food) affects the development of and reverses the ventricular hypertrophy in deoxycorticosterone acetate (DOCA) (8 mg/kg SC twice a week)-salt hypertensive rats. Chlorthalidone was given to one group during all 20 days of DOCA administration (preventive regimen) and to another group 20 days after DOCA treatment was initiated until the 40th day (therapeutic regimen). Chlorthalidone was found to reduce or prevent the development of ventricular hypertrophy, as assessed by a reduction in ventricular mass and cardiac protein as well as arterial hypertension. Both chlorthalidone regimens prevented the increase or induced a significant decrease in the plasma concentration of sodium and in cardiac sympathetic tone, which were both increased in DOCA-salt-treated rats. These data provide evidence that long-term chlorthalidone treatment is effective in preventing or reducing ventricular hypertrophy along with arterial hypertension. However, whether this is due to a reduction in plasma sodium or other additional mechanisms, such as a reduction in cardiac sympathetic tone, remains to be determined.

Time course of cardiac sympathetic and vagal tone changes in renovascular hypertensive rats.

The present study has examined the time course of autonomic tone changes in two-kidney, one-clip (2K1C) and one-kidney, one-clip (1K1C) renal hypertension. In conscious rats, cardiac sympathetic and vagal tone were determined using propranolol and atropine, respectively. The development of renovascular hypertension was accompanied by a significant tachycardia, increase in cardiac sympathetic tone and decrease in cardiac vagal tone. In the isolated perfused heart we observed a reduced chronotropic response to isoproterenol. These alterations were transitory in 2K1C and greater and more persistent in 1K1C renal hypertension. These results show the relative role played by the cardiac sympathetic and vagal systems in the maintenance of tachycardia in renovascular hypertension.

Evidence that the autonomic nervous system plays a major role in the L-NAME-induced hypertension in conscious rats.

The present study was designed to investigate the role of the autonomic nervous system in experimental hypertension induced by chronic administration of N-nitro-L-arginine methyl ester (L-NAME) in the drinking water (1 mg/mL) over 6 days. L-NAME ingestion caused a large rise in resting mean arterial pressure (MAP) (175 +/- 5 mm Hg) and heart rate (HR) (440 +/- 17 beats per minute) compared to nontreated control rats (resting MAP: 112 +/- 2 mm Hg and HR: 345 +/- 8 beats per minute). Ganglionic blockade induced by trimethaphan (5 mg/kg, intravenously) caused a significantly (P < .01) greater decrease in MAP (delta -86 +/- 7 mm Hg) compared to control rats MAP (delta -44 +/- 4 mm Hg). This strongly suggests that the level of central sympathetic tone in L-NAME-treated rats is much greater than in nontreated rats. Using atenolol and atropine alone and combined, the level of resting sympathetic drive to the heart was found to be significantly increased in L-NAME-treated rats compared to control rats. However, vagal tone to the heart was found to be virtually abolished in L-NAME-treated rats compared to control rats. These results indicate that an increase in central sympathetic drive plays an important role in the hypertension induced by chronic inhibition of nitric oxide synthesis with L-NAME.

Inhibition of nitric oxide synthase causes profound enhancement of the Bezold-Jarisch reflex.

The Bezold-Jarisch reflex function was evaluated in rats made hypertensive by the chronic oral intake of a nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME, averaging 35 mg/kg/day), for 3, 6, and 12 days (n = 9/group) and in untreated control rats (CR, n = 9/group). L-NAME-treated rats showed a marked hypertension (MAP: 148 +/- 3, 182 +/- 4, and 179 +/- 4 mm Hg, respectively) compared with CR (110 +/- 2 mm Hg). The 6- and 12-day groups showed tachycardia (447 +/- 20 and 466 +/- 13 beats/min, respectively) when compared with CR (355 +/- 10 beats/min). When compared with CR, left ventricular hypertrophy was observed in rats treated with L-NAME for 6 and 12 days. The Bezold-Jarisch reflex, a decrease in heart rate (HR) accompanied by a decrease in diastolic arterial pressure (DAP), was evoked in a dose dependent manner by the intravenous injection of 5-hydroxytryptamine (5-HT, 5 to 10 microg/kg). Relative to responses observed in CR, 5-HT at 10 microg/kg caused a four- to fivefold greater decrease in HR and a two- to threefold greater decrease in DAP in all the L-NAME treatment groups. Using a Langendorff technique, we observed a significant increase in the responsiveness of the pacemaker to acetylcholine (1.25 to 80 microg/mL). These data suggest that the pharmacological inhibition of the nitric oxide synthase causes profound changes in the mechanisms of cardiovascular regulation as shown by a marked enhancement of the Bezold-Jarisch reflex in L-NAME-treated rats. The enhancement of this reflex seems to be in great part due to the hyperresponsiveness of the cardiac pacemaker to cholinergic stimulation.

Effects of verapamil on blood pressure and heart rate in neurogenic hypertensive rats.

The effects of verapamil (220 micrograms/kg per min i.v.) on blood pressure and heart rate were studied in sinoaortic baroreceptor denervated and sham-operated rats. In the conscious animals the verapamil-induced hypotension was accompanied by a significant heart rate increase in the first group (from 352 +/- 7 to 422 +/- 10 beats/min) and a decrease in the second group (from 485 +/- 13 to 400 +/- 9 beats/min). The verapamil-induced tachycardia observed in sham-operated rats was prevented by atropine plus propranolol but not by adrenal demedullation. Tachycardia was present in urethane-anesthetized sham-operated rats, similar to the sinoaortic baroreceptor-denervated rats. After verapamil a significant heart rate reduction was observed in sham-operated but not in sinoaortic baroreceptor-denervated rats. The results in conscious rats suggest that the direct inhibitory action of this drug on sinus node automaticity is suppressed by baroreflex tachycardia and that anesthesia masks this response.

Chlordiazepoxide and morphine reduce pressor response to brain stimulation in awake rats.

The effects of intravenous as well as dorsal midbrain injections of morphine and chlordiazepoxide on the blood pressure rise induced by electrical stimulation of the dorsal periaqueductal gray matter (DPAG) were studied in unanesthetized rats. Chlordiazepoxide applied systemically or locally into the DPAG, as well as locally applied but not systemically injected morphine were found to attenuate the centrally-induced hypertension. These data together with others suggest that benzodiazepines as well as local injections of morphine into the DPAG decrease the aversive effect induced by DPAG stimulation.

Chronic activation of central alpha2-adrenoceptors prevents hypertension in DOCA-salt rats.

The effects of chronic intracerebroventricular (i.c.v.) injections of the alpha2-adrenoceptor agonist, xylazine, on blood pressure were examined in DOCA-salt rats. Acute studies also examined the renal sympathetic nerve activity (RSNA) and renal excretory responses produced by i.c.v. xylazine in rats with established DOCA-salt hypertension. Rats implanted with a chronic i.c.v. cannula for drug injection were used. In chronic studies, four groups were investigated: control rats treated with s.c. soybean oil and i.c.v. saline; DOCA-salt rats (s.c. deoxycorticosterone acetate) receiving i.c.v. saline, xylazine or the alpha2-adrenoceptor antagonist, yohimbine. During vehicle or DOCA-salt treatment, xylazine (0.2 ng/microg) or yohimbine (10O microg/kg) was injected i.c.v. daily (three times). In DOCA-salt rats receiving i.c.v. saline, resting mean arterial pressure (MAP) was elevated on days 15 and 30 (135 +/- 5 and 160 +/- 6 mmHg, respectively). Chronic i.c.v. xylazine significantly attenuated the rise in MAP produced by DOCA-salt (day 15, 118 +/- 5 mmHg; day 30, 121 +/- 4 mmHg). Alternatively, chronic i.c.v. yohimbine shortened the onset (day 15, 152 +/- 7 mmHg) and augmented the hypertension in DOCA-salt rats (0 survival by day 30). In acute studies, i.c.v. xylazine elicited a profound natriuresis and diuresis as well as a reduction in RSNA without altering MAP. This study demonstrates that the ongoing (tonic) activity of central alpha2-adrenoceptor mechanisms are critically involved in regulating blood pressure in the DOCA-salt treated rat. In this manner, an enhanced activity of central alpha2-adrenoceptor systems acts to protect against a rise in blood pressure. In contrast, the attenuation of central alpha2-adrenoceptor stimulation evokes hypertension. The central action of xylazine to prevent hypertension may be associated with the inhibition of sympathetic outflow to the kidneys and evokes an enhanced natriuresis. By inhibiting the avid sodium retention elicited by DOCA-salt treatment, the central activation of alpha2-adrenoceptors delays the onset and the severity of hypertension in this pathological model.

Influence of a multideficient diet from northeastern Brazil on resting blood pressure and baroreflex sensitivity in conscious, freely moving rats.

The "regional basic diet" or RBD is a multideficient diet (providing 8% protein) which is known to produce dietary deficiencies in some populations in northeastern Brazil. The present study investigated the effects of RBD-induced malnutrition on resting blood pressure and baroreflex sensitivity in conscious rats. Malnourished rats were obtained by feeding dams the RBD during mating and pregnancy (RBD-1 group) or during nursing and a 10-day period after weaning (RBD-2 group). At 90 days of age, only RBD-2 rats weighed significantly (P<0.001) less than control rats born to dams fed a standard commercial diet (23% protein) during pregnancy and nursing. Baseline mean arterial pressure and heart rate of both RBD-1 and RBD-2 rats were comparable to those of controls. The slopes for both reflex bradycardia and tachycardia (bpm/mmHg) induced by intravenous phenylephrine and sodium nitroprusside, respectively, were unchanged in either RBD-1 (-2.08 +/- 0.11 and -3.10 +/- 0.43, respectively) or RBD-2 (-2.32 +/- 0.30 and -3.73 +/- 0.53, respectively) rats, when compared to controls (-2.09 +/- 0.10 and -3.17 +/- 0.33, respectively). This study shows that, after a prolonged period of nutritional recovery, the patterns of resting blood pressure and baroreflex sensitivity of both pre- and postnatally malnourished rats were similar to those of controls. The decreased body weight and the tendency to increased reflex tachycardia in RBD-2 rats may suggest that this type of maternal malnutrition during lactation is more critical than during pregnancy.

Baroreceptor reflex function in rats submitted to chronic inhibition of nitric oxide synthesis.

1. The chronic inhibition of nitric oxide synthesis by N omega-nitro-L-arginine-methyl ester (L-NAME) leads to arterial hypertension accompanied by a significant increase in cardiac sympathetic tone and an almost complete abolition of the vagal tone in conscious adult male Wistar rats. The main aim of the present study was to examine the baroreceptor heart rate reflex function in L-NAME-treated rats (N = 10). 2. Spontaneous daily oral intake of L-NAME (1 mg/ml for 6 days) caused marked hypertension and tachycardia (176 +/- 5 mmHg and 418 +/- 16 bpm), when compared to untreated rats (111 +/- 2 mmHg and 354 +/- 8 bpm). 3. Baroreflex gain was determined in conscious freely moving rats by sigmoidal curve fitting analysis using alternate intravenous injections of phenylephrine (0.2-10.0 micrograms/kg) and sodium nitroprusside (0.5-20.0 micrograms/kg) to produce pressor-induced bradycardia and depressor-induced tachycardia, respectively. The baroreflex gain (sensitivity) was significantly enhanced in L-NAME-treated rats compared to control rats (10.9 +/- 2.5 vs 4.5 +/- 0.3 bpm/mmHg, respectively) mainly due to exaggerated reflex bradycardia responses to increases in arterial hypertension. 4. The data indicate that chronic inhibition of nitric oxide synthesis enhances the bradycardic component of the baroreflex function.

Impairment of the Bezold-Jarisch reflex in conscious rats with myocardial hypertrophy.

The aim of the present investigation was to study the Bezold-Jarisch reflex in catecholamine-induced myocardial hypertrophy. Ten conscious male albino rats (260-300 g) were treated for 15 days with isoproterenol (IR), 0.3 mg/kg injected im once a day, and compared to 10 control rats (CR) similarly injected with vehicle (0.25 ml). No significant changes in body weight, resting mean arterial pressure or heart rate were observed in the IR group. Left and right ventricular hypertrophy was observed in IR animals (27% and 28%, respectively, P < 0.01) when compared to CR. The Bezold-Jarisch reflex was tested by injecting 5-hydroxytryptamine (4-32 micrograms/kg, iv) and was characterized by a simultaneous fall in diastolic arterial pressure (for example: 91 +/- 4 to 61 +/- 3 mm Hg, 16 micrograms/kg) and bradycardia (for example: 330 +/- 10 to 177 +/- 25 bpm, 16 micrograms/kg). This reflex was significantly attenuated in the IR when compared to the CR group. Our data suggest that ventricular hypertrophy without changes in arterial pressure can lead to a reduction of the Bezold-Jarisch reflex. The results reported here are in agreement with other studies showing that the impairment of cardiopulmonary reflex in hypertensive animals and humans occurs exclusively when the hypertension is accompanied by ventricular hypertrophy.

Chronic experimental myocardial infarction produces antinatriuresis by a renal nerve-dependent mechanism.

The present study focused on the role of sympathetic renal nerve activity, in mediating congestive heart failure-induced sodium retention following experimental chronic myocardial infarction. Groups of male Wistar rats (240-260 g) were studied: sham-operated coronary ligation (CON3W, N = 11), coronary ligation and sham-operated renal denervation (INF3W, N = 19), 3 weeks of coronary ligation and sympathetic renal nerve denervation (INF3WDX, N = 6), sham-operated coronary ligation (N = 7), and 16 weeks of coronary ligation (INF16W, N = 7). An acute experimental protocol was used in which the volume overload (VO; 5% of body weight) was applied for 30 min after the equilibration period of continuous iv infusion of saline. Compared to control levels, VO produced an increase (P < 0.01, ANOVA) in urine flow rate (UFR; 570%) and urinary sodium excretion (USE; 1117%) in CON3W. VO induced a smaller increase (P < 0.01) in USE (684%) in INF3W. A similar response was also observed in INF16W. In INF3WDX, VO produced an immediate and large increase (P < 0.01) in UFR (547%) and USE (1211%). Similarly, in INF3W VO increased (P < 0.01) UFR (394%) and USE (894%). Compared with INF3W, VO induced a higher (P < 0.01) USE in INF3WDX, whose values were similar to those for CON3W. These results suggest that renal sympathetic activity may be involved in sodium retention induced by congestive heart failure. This premise is supported by the observation that in bilaterally renal denervated INF3WDX rats myocardial infarction was unable to reduce volume expansion-induced natriuresis. However, the mechanism involved in urinary volume regulation seems to be insensitive to the factors that alter natriuresis.

Left ventricular hypertrophy differences between male and female renovascular hypertensive rats.

In a previous study we demonstrated ventricular hypertrophy in male but not in female sinoaortic denervated rats. To evaluate a possible sexual influence on ventricular hypertrophy of other models for experimental hypertension, we studied two-kidney one clip and one-kidney one clip Goldblatt hypertension. The results showed left ventricular hypertrophy in male but not in female two-kidney one clip groups, despite the same arterial hypertension level in both groups. In the one-kidney one clip groups, left ventricular hypertrophy was greater in male than in female rats. The results indicate a sexual influence in ventricular hypertrophy when the arterial renovascular hypertension level is moderate.

Reduction of contractile performance in the myocardium from unilaterally nephrectomized rats.

The contractile performance of left ventricle papillary muscles from sham operated controls and uninephrectomized rats was investigated using isometric contractions. The results suggest that unilateral nephrectomy induces a decrease in the developed tension of the papillary muscles characterizing a reduction in contractility.