Evaluation of antimicrobial edible coatings from a whey protein isolate base to improve the shelf life of cheese.

The objective of this work was to evaluate the effectiveness of antimicrobial edible coatings to wrap cheeses, throughout 60 d of storage, as an alternative to commercial nonedible coatings. Coatings were prepared using whey protein isolate, glycerol, guar gum, sunflower oil, and Tween 20 as a base matrix, together with several combinations of antimicrobial compounds-natamycin and lactic acid, natamycin and chitooligosaccharides (COS), and natamycin, lactic acid, and COS. Application of coating on cheese decreased water loss (~10%, wt/wt), hardness, and color change; however, salt and fat contents were not significantly affected. Moreover, the antimicrobial edible coatings did not permit growth of pathogenic or contaminant microorganisms, while allowing regular growth of lactic acid bacteria throughout storage. Commercial nonedible coatings inhibited only yeasts and molds. The antimicrobial edible coating containing natamycin and lactic acid was the best in sensory terms. Because these antimicrobial coatings are manufactured from food-grade materials, they can be consumed as an integral part of cheese, which represents a competitive advantage over nonedible coatings.

Emergent food proteins - Towards sustainability, health and innovation.

There is an increasing demand for alternative and sustainable protein sources, such as vegetables, insects and microorganisms, that can meet the nutritional and sensory pleasantness needs of consumers. This emergent interest for novel protein sources, allied with "green" and cost-effective processing technologies, such as high hydrostatic pressure, ohmic heating and pulsed electric fields, can be used as strategies to improve the consumption of proteins from sustainable sources without compromising food security. In addition to their nutritional value, these novel proteins present several technological-functional properties that can be used to create various protein systems in different scales (i.e., macro, micro and nano scale), which can be tailored for a specific application in innovative food products. However, in order for these novel protein sources to be broadly used in future food products, their fate in the human gastrointestinal tract (e.g., digestion and bioavailability) must be assessed, as well as their safety for consumers must be clearly demonstrated. In particular, these proteins may become novel allergens triggering adverse reactions and, therefore, a comprehensive allergenicity risk assessment is needed. This review presents an overview of the most promising alternative protein sources, their application in the production of innovative food systems, as well as their potential effects on human health. In addition, new insights on sustainable processing strategies are given.

Diabetes mellitus and hypertension. State of the art lecture.

In rats with streptozotocin-induced diabetes an increase in arterial blood pressure was observed as early as the first week after the drug was injected. Blood pressure reached maximal values around the fourth week and remained stable for a long period of follow-up. The responsiveness of these rats to the three major vasopressor hormones, angiotensin II, norepinephrine, and vasopressin, was decreased in the early phase of diabetes and returned to normal in the late phase. Acute treatment at the third, sixth, and twelfth weeks with blockers of these vasopressor hormones resulted in a significant fall in blood pressure at the third week with captopril and at the twelfth week with propranolol plus phentolamine. No significant fall was observed when a specific vasopressin inhibitor was administered. Good control of the blood pressure was obtained when these rats were treated chronically with captopril or prazosin, and partial control was achieved when they were fed a low salt diet. An attenuation in arterial blood pressure levels was observed in rats with two-kidney, one clip hypertension when diabetes was induced by streptozotocin. Plasma creatine levels in diabetic rats were significantly higher than those in control rats only in the sixth and twelfth weeks. Electron microscopy revealed some minor glomerular lesions only at the twelfth week.

Effects of systemic hypertension, antidiuretic hormone, and prostaglandins on remnant nephrons.

Renal function was evaluated in normal and after 30 days of 5/6 renal mass reduction (CRF) in Munich-Wistar (MW) rats, spontaneously hypertensive rats with superficial glomeruli (EPM), and in Brattleboro rats with congenital diabetes insipidus (DI). Mean arterial pressure was higher in EPM-Control and EPM-CRF rats as compared with MW and DI rats. MW and EPM rats with CRF showed increases of 120% and 196%, respectively, in single nephron glomerular filtration rate as compared with their controls. However, DI rats with CRF did not show any increase in single nephron glomerular filtration rate as compared with the control group. Therefore, the data suggest that the presence of hypertension enhances the adaptive mechanisms on remnant kidney's function. Conversely, in the absence of antidiuretic hormone, adaptive mechanisms of remnant nephrons did not occur. In addition, it was observed that rats with CRF submitted to prostaglandin blockade with indomethacin showed for MW rats a 55% and 20% reduction in ultrafiltration coefficient and in single nephron glomerular filtration rate, respectively. Decreases of 60% and 30% in ultrafiltration coefficient and single nephron glomerular filtration rate, respectively, were observed for EPM rats. In contrast, DI rats did not show any alteration on renal function after indomethacin. It seems, therefore, that prostaglandins play a role in remnant nephron function of MW and EPM rats, but in the absence of antidiuretic hormone, prostaglandins do not affect remnant glomerular hemodynamics.

Effects of cyclooxygenase inhibitors on plasma and urinary kallikrein.

In vitro studies were performed to investigate the direct effects of the cyclooxygenase inhibitors (COI), meclofenamate, imidazol, acetylsalicylic acid (ASA), indomethacin, and acetaminophen on the plasma kallikrein system and on urinary kallikrein excretion. Biological (guinea pig ileum) and colorimetric (synthetic substrate) methods were used. Results showed that all COIs except ASA affected both the activation of pre-kallikrein in plasma and the direct activity of plasma kallikrein, but none of the COIs tested was able to alter the urinary kallikrein excretion. Additionally, in Wistar rats we studied the effects of chronic administration of ASA, meclofenamate, and indomethacin on the plasma kallikrein system and urinary kallikrein excretion. In contrast to the in vitro studies, administration of these COIs reduced the amount of total 24-hour urinary kallikrein excretion. Moreover, the pre-plasma kallikrein and total plasma kallikrein levels were diminished in all experimental groups. However, only ASA and meclofenamate increased the free-plasma kallikrein levels despite the fact the three COIs used reduced the high molecular weight kininogen. Thus, in vitro data suggest an important and direct effect of meclofenamate, imidazol, indomethacin, and acetaminophen on the plasma kallikrein system, without any effect on urinary secretion. ASA was the only COI that showed no direct effect in these experiments. Chronic COI administration in Wistar rats suggests that ASA, meclofenamate, and indomethacin affect both the plasma kallikrein-kinin system and kallikrein excretion. When these drugs are used to evaluate the interactions between prostaglandins and the kallikrein-kinin system, their possible effects through both mechanisms, directly or via prostaglandin inhibition, should be considered.

Hemodynamic mechanism of blood pressure response to captopril in human malignant hypertension.

The hemodynamic mechanism of blood pressure response to angiotensin blockade is well established in "benign" but not in human malignant hypertension. We studied the changes in mean arterial pressure (MAP), cardiac index (CI), pulmonary wedge pressure (PWP), and in plasma volume (PV) induced by a single oral dose of captopril (150 mg) in 11 patients with malignant hypertension. Two hours after captopril, MAP fell from 178.5 +/- 5.8 to 151.8 +/- 7.8 mm Hg (p less than 0.001) (means +/- SEM) due to a fall in total peripheral resistance (TPR) (from 54.8 +/- 6.8 to 46.4 +/- 1.6 arbitrary units, p less than 0.001). However, there was a simultaneous increase in CI (from 3.29 +/- 0.13 to 3.70 +/- 0.15 liter/min/m2, p less than 0.001), and a decrease in PWP (from 15.3 +/- 3.5 to 11.0 +/- 2.5 mm Hg, p less than 0.001), while PV remained unchanged (from 4.02 +/- 0.26 to 4.12 +/- 0.12 liters, n.s.). Our data show that, in human malignant hypertension, blood pressure response to captopril is due to a decrease in TPR, but in contrast to benign hypertension, there is also a simultaneous increase in CI. Our results suggest that, in malignant hypertension, potentially high CI levels are artificially normalized by the increased TPR and may be fully disclosed by vasodilation.

Anteroventral third ventricle and renin-angiotensin system interaction in the two-kidney, one clip hypertensive rat.

To test the peripheral mechanisms of prevention and reversal of two-kidney, one clip (2K1C) hypertension in the rat by lesion of the anteroventral third ventricle (AV3V) region, we studied blood pressure responses in rats to AV3V lesion produced before (n = 8) or after (n = 8) clipping the left renal artery. Two groups of sham-lesioned, clipped rats (n = 9 each) served as controls. At the end of the experiments, saralasin and captopril were given to evaluate the angiotensin-dependent component of blood pressure. To study the influence of the procedures on plasma renin activity (PRA), two parallel groups of rats (n = 26 and 24, respectively) were submitted to similar surgical protocols. We observed that increases in blood pressure were significantly smaller in the previously lesioned compared to previously sham-lesioned animals (delta BP = 21.5 +/- 3.7 vs. 32.9 +/- 2.5 mm Hg, p less than 0.01); also, AV3V lesion almost completely reversed hypertension (BP from 167.5 +/- 2.9 to 136.0 +/- 4.1 mm Hg, p less than 0.001), which was not observed in the sham-lesioned animals (BP from 172.0 +/- 2.8 to 168 +/- 2.7 mm Hg, NS). Saralasin produced a significantly smaller decrease in BP in the lesioned animals compared to those with sham lesions during both prevention and reversal experiments. Similar results were observed with captopril. Previous AV3V lesion did not significantly affect PRA with clipping of the renal artery, but AV3V destruction after hypertension had been established resulted in significantly lower PRA compared to sham-lesioned animals (4.58 +/- 0.72 vs 8.38 +/- 1.79, respectively, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Methylprednisolone-induced hypertension. Role for the autonomic and renin angiotensin systems.

The role of the autonomic nervous system (ANS) in the pathogenesis of hypertension induced by methylprednisolone (20 mg/kg/week subcutaneously) was studied in rats before and during chronic renin angiotensin system (RAS) blockade with captopril (20 mg/kg/every 8 hrs by mouth). Sympathetic nervous system (SNS) blockade was accomplished by the intravenous (i.v.) administration of propranolol (0.20 mg/100g) plus phentolamine (1.25 mg/100g/i.v.) and ganglionic (G) blockade by the use of pentolinium tartarate (0.5 mg/100g/i.v.). After 4 weeks, methylprednisolone-treated animals showed significant decreases in mean arterial pressure (MAP) with both SNS (-34 +/- 2 mm Hg) and G (-56 +/- 3 mm Hg) blockades; during chronic RAS blockade, even greater falls in MAP were observed (SNS = -43 +/- 2 mm Hg and G = -75 +/- 3 mm Hg). Nevertheless, for both groups the levels of MAP obtained during SNS and G blockades were higher than those observed in their control groups. At the end of second week, however, in captopril-treated hypertensive rats the values of MAP obtained during ANS blockade were lower than those observed in the control group. An increased responsiveness to exogenous administration of norepinephrine (NE) was observed in animals receiving methylprednisolone and captopril. It is concluded that methylprednisolone hypertension in the rat may be initially explained by activation of RAS and ANS. At later phases, a third mechanism has to be postulated to explain the hypertensive state.

Role of the anteroventral third ventricle region and the renin angiotensin system in methylprednisolone hypertension.

Methylprednisolone (M, 10 mg/kg/week subcutaneously) was administered to cause hypertension in rats, and the role of AV3V region was assessed before and after development of the hypertensive state. Participation of the renin angiotensin system (RAS) was evaluated by changes in mean arterial pressure (MAP) induced by administration of saralasin (S, 10 micron g/kg/min i.v.) or captopril (C, 20 mg/kg/p.o).aAnaAV3V lesion before M administration partially prevented and delayed the beginning appearance of M hypertension. Furthermore, a prior AV3V lesion abolished an angiotensin II (AII)-dependent pressor component normally identified by S and C administration in this type of hypertension. During the maintenance phase of the hypertension, an AV3V lesion caused a partial reduction in blood pressure. A spontaneous disappearance of a vasoconstrictor component mediated by AII was observed in the late phases of M hypertension. It is concluded that the AV3V region is essential to the full development and maintenance of M hypertension in the rat. Also in this model, integrity of the AV3V area is essential to the expression of the AII-mediated pressor component. Finally it is apparent tha M can cause hypertension even in the absence of the AV3V area or during chronic renin angiotensin blockade, indicating multiple pathogenetic mechanisms in this experimental model.

Pindolol, not propranolol, reverses cardiac hypertrophy in renal hypertensive rats.

Reversal of cardiac hypertrophy has been obtained by treatment with some antihypertensive drugs but has not been achieved consistently with beta blockers. To investigate whether this difference might be explained by the distinct hemodynamic actions of the drugs, we studied the effects of propranolol and pindolol, beta blockers with distinct modes of action, on cardiac hypertrophy of hypertensive male Wistar rats, two-kidney, one clip (2K1C) Goldblatt model (n = 33) and sham-operated control rats (n = 34). We also assessed the effects of such therapies on the ventricular pumping ability during open-chest, transient aortic occlusion. Four weeks after surgery, propranolol (5 mg/kg/day p.o.) was given to hypertensive (n = 8) and control rats (n = 11); pindolol was also given orally (1 mg/kg/day) to similar groups (n = 7 and n = 5, respectively). Untreated animals served as controls for both groups. Cardiac hypertrophy developed with hypertension in the untreated rats of the propranolol (3.38 +/- 0.18 vs 2.60 +/- 0.08 mg/g; p less than 0.01) and pindolol groups (3.93 +/- 0.21 vs 2.40 +/- 0.03 mg/g; p less than 0.001). Treatment reversed cardiac hypertrophy in the pindolol-treated (3.01 +/- 0.19 vs 3.93 +/- 0.21 mg/g; p less than 0.001, NS) but not in the propranolol-treated rats (3.24 +/- 0.18 vs 3.38 +/- 0.21 mg/g, NS). The maximal pressure that developed during aortic occlusion in the propranolol group was similar to that observed in the pindolol group. These results indicate that cardiac hypertrophy is reversed by pindolol but not by propranolol, and that this reversal does not interfere with left ventricular pumping ability.

Rapid eye movement sleep deprivation and hypertension. Genetic influence.

We studied the importance of genetic predisposition in the development of stress-induced hypertension in the spontaneously hypertensive rat (SHR), Wistar-Kyoto (WKY) rat, and borderline hypertensive rat (BHR; first-generation offspring of SHR and WKY). Rats were submitted to seven 72-hour sessions of rapid eye movement sleep deprivation (REM-sd) every other week during 13 weeks. Tail arterial pressure was determined throughout the experiment. At the end of the study, mean arterial pressure (direct measurement), sympathetic activity (acute blockade with propranolol and phentolamine), and ventricular weight were determined. Results showed that REM-sd induced sustained hypertension only in rats with a partial predisposition to developing hypertension (BHRs). Values of tail arterial pressure at the end of the study were BHR REM-sd, 175 +/- 1.6 mm Hg and control BHR, 155.9 +/- 0.9 mm Hg, p less than 0.05; SHR REM-sd, 219 +/- 2.6 mm Hg and control SHR, 211.9 +/- 3.4 mm Hg, NS; WKY REM-sd, 123.9 +/- 2 mm Hg and control WKY, 125.4 +/- 2.2 mm Hg, NS. Stressed groups showed higher reduction of mean arterial pressure than their controls when submitted to sympathetic blockade (SHR REM-sd, -75.7 +/- 13.2 mm Hg and control SHR, -60 +/- 4.5 mm Hg, p less than 0.05; BHR REM-sd, -38.4 +/- 3.6 mm Hg and control BHR, -24.3 +/- 2.1 mm Hg, NS; WKY REM-sd, -34.4 +/- 2.5 mm Hg and control WKY, -25.6 +/- 3.3 mm Hg, NS). REM-sd increased ventricular weight in all strains. These increments showed no correlation with blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Severe hypertension induces disturbances of renal autoregulation.

To study if the severity of hypertension could be associated with disturbances of the autoregulation of renal blood flow and glomerular filtration, we compared the renal hemodynamic and functional responses to acute blood pressure reductions of a group of patients with moderate essential hypertension (n = 10) with those of a group of patients with severe hypertension (n = 10). Blood pressure was reduced to normal levels by a stepwise infusion of sodium nitroprusside, and effective renal blood flow (by 131I-hippuran), glomerular filtration rate (by endogenous creatinine clearance), and filtration fraction were determined. After acute blood pressure normalization, effective renal blood flow and glomerular filtration rate were significantly reduced in patients with severe hypertension (-41.6 +/- 8.3% and -44.7 +/- 6.8%, respectively; p less than 0.01 for both) but not in those with moderate hypertension (+4.9 +/- 9.1% and +6.2 +/- 13.3%, respectively; NS). Filtration fraction remained unchanged in both groups. These results show that severe but not moderate essential hypertensive patients have a displacement to the right of the lower limit of the renal autoregulation curve due to impaired vasodilation to maintain adequate renal blood flow during acute reductions of blood pressure. This impairment may be due to anatomic or functional defects of preglomerular vessels, or to both. Furthermore, the inability to maintain adequate glomerular filtration in these circumstances shows that patients with severe hypertension also have an impaired ability to adjust postglomerular vasomotor tone in the face of reductions in glomerular blood flow.

Role of substance P in blood pressure regulation in salt-dependent experimental hypertension.

The participation of substance P in the pathogenesis of five models of experimental hypertension, ie, DOCA-salt, subtotal nephrectomy, one-kidney-one clip renovascular, two-kidney-one clip renovascular, and spontaneous hypertension, was evaluated via an acute infusion of a newly synthesized potent, specific nonpeptide antagonist of substance P at the NK-1 receptor, the agent CP 96,345. In conscious unrestrained rats, CP 96,345 induced significant and sustained increases in mean arterial pressure of DOCA-salt, subtotal nephrectomy, and one-kidney-one clip renovascular hypertensive rats but only small and nonsignificant changes in blood pressure of two-kidney-one clip renovascular and spontaneously hypertensive rats. CP 96,345 had no effect on the blood pressure of sham-treated controls and Wistar-Kyoto rats. This NK-1 receptor antagonist did not significantly affect the heart rate of any experimental model studied. The data suggest that endogenous substance P may act as a partial counterregulatory mechanism against vasoconstriction in models of salt-dependent hypertension.

Cardiovascular effects of a specific nonpeptide antagonist of substance P (NK-1) receptor in DOCA-salt hypertension.

The neurotransmitter substance P acts also as a potent vasodilator. Its participation in the pathogenesis of deoxycorticosterone acetate (DOCA)-salt hypertension was evaluated by an acute infusion of a newly synthesized, potent, specific nonpeptide antagonist of substance P at the NK-1 receptor, the agent CP 96,345. In conscious unrestrained rats, CP 96,345 induced significant and sustained increases in mean arterial pressure of DOCA-salt rats but only small, transient, and nonsignificant rises in blood pressure of sham-treated control rats. The rise in blood pressure was not accompanied by changes in heart rate. Maximal blood pressure increase in DOCA-salt rats was 31.7 +/- 14.8 mm Hg. In a second series of experiments, the hemodynamic effects of this antagonist were evaluated under anesthesia in both DOCA-salt and sham-treated control rats by the thermodilution method. During CP 96,345 infusion, sustained increases in cardiac index and stroke volume and decreases in total peripheral resistance were observed in both DOCA-salt and control rats. In DOCA-salt rats, cardiac index rose by 79.4%, while total peripheral resistance fell by 27.9% of the baseline values. In control rats, the changes were smaller (+27.2% and -22.5%, respectively). Stroke volume changed in parallel to cardiac output in both groups. The data suggest that acute blockade of NK-1 receptors increases blood pressure in DOCA-salt rats mainly by an increase in cardiac output. We conclude that endogenous substance P tends to counteract the DOCA-salt-induced elevation of blood pressure by modulating both cardiac output and peripheral resistance.

Malignant hypertension: a syndrome accompanied by plasmatic diminution of low and high molecular weight kininogens.

Total kininogen (Kgn), kallikrein, and prekallikrein were measured in patients with malignant hypertension (MH), essential hypertension (EH), normotensive control (NC), and hypertension and chronic renal failure (HRF). These components of the kallikrein-kinin system were related to the levels of creatinine and fibrinogen. High molecular weight Kgn and low molecular weight Kgn were also measured in blood samples from a peripheral vein, arterial blood, and suprahepatic vein in NC, EH, and MH. Results showed that total Kgn levels were diminished in MH and this diminution could not be ascribed to decreases in renal function, hematocrit, or fibrinogen levels. Appropriate antihypertensive treatment for over 1 year did not normalize Kgn levels in 10 of 11 patients. High molecular weight Kgn and low molecular weight Kgn were both diminished in MH (0.26 +/- 0.04 nmol bradykinin/ml and 0.93 +/- 0.12 nmol lysyl-bradykinin/ml, respectively) as compared to NC (0.39 +/- 0.07 and 1.92 +/- 0.16) and EH (0.51 +/- 0.07 and 1.65 +/- 0.13). Higher concentrations of high molecular weight Kgn were demonstrated in the suprahepatic vein as compared to arterial blood, demonstrating its synthesis by the liver. However, patients with MH had a diminished capacity to synthetize high molecular weight Kgn. A decrease in synthesis of high molecular weight Kgn may be a partial explanation for low levels of total Kgn. It is suggested that a lack of Kgn may play a role in the pathogenesis of MH.

Dynamic evaluation of prolactin secretion in essential hypertension: evidence against hypothalamic-pituitary dopaminergic dysfunction.

Hyperprolactinemia has previously been noted in patients with essential hypertension and it has been suggested that the increased PRL levels in this condition may reflect reduced central dopaminergic activity. In the present study, PRL secretion was evaluated in 17 patients with essential hypertension and in 9 normal controls as an indirect index of hypothalamic-pituitary dopaminergic activity. PRL levels were measured basally, at night, and after TRH (200 micrograms, iv), metoclopramide (10 mg, orally), and L-dopa (500 mg, orally). Basal PRL levels were similar in both groups [essential hypertension, 301.2 +/- 176.2 microunits/ml; controls, 334.2 +/- 98.8 microunits/ml (mean +/- SD)]. No differences in PRL levels were found after TRH, L-dopa, and metoclopramide or during sleep between the 2 groups. When the patients were classified according to their PRA, no differences were noticed in either basal levels or the patterns of PRL response. It is concluded that PRL secretion is normal in patients with essential hypertension, which could be indirect evidence against reduced hypothalamic-pituitary dopaminergic activity in this disease. However, minor abnormalities not detected by PRL measurements could be involved in the pathogenesis of essential hypertension.

Hypertension and economic activities in São Paulo, Brazil.

A study of the prevalence of hypertension was undertaken among workers in 10 subsectors of the economy in São Paulo, a major urban-industrial area of Brazil. Included in the study were 5500 subjects 15-65 years of age, employed in 57 randomly selected firms. Hypertension rates (DBP greater than or equal to 90 mm Hg) were higher among males up to 44 years of age. There was a decreasing gradient from mild to moderate and severe forms in all groups. Severity tended to increase with age in all groups. Black males showed higher rates than whites (29.2% vs 16.7%, p less than 0.05), the excess being partially accounted for by moderate and severe forms (40% vs 20%). Subjects who overworked showed a trend toward higher hypertension rates. Higher rates in four subsectors (metallurgy, finance, transport, and journalism), aside from the distribution of known risk factors and job selection, may reflect a variety of work-related stressors.

Acute hemodynamic and humoral effects of metoclopramide on blood pressure control improvement in subjects with diabetic orthostatic hypotension.

Metoclopramide (MCP), a dopaminergic antagonist, is effective in postural hypotension, but the mechanisms of action have not been well defined. We studied responses of mean arterial pressure (MAP), heart rate, cardiac output (CO), and total peripheral resistance (TPR) after 5 min of increasing degrees of head tilt (15 degrees to 90 degrees) before and after MCP (20 mg IV) in seven subjects with diabetic postural hypotension. Plasma renin activity (PRA) and plasma aldosterone levels (PA) were determined at each degree of tilt; responses to the cold pressor test were also assessed before and after MCP. Before MCP, the maximal degree of tilt tolerated was 75 degrees, while after MCP four subjects were able to support 90 degrees tilt. At 45 degrees tilt, the decreases in MAP were smaller after than before MCP (-7.6 +/- 3.3 and -28.1 +/- 8.5 mm Hg; means +/- SE). This was associated with responses of TPR to tilt after (from 18.6 +/- 2.6 to 24.0 +/- 3.9 arbitrary units [AU]) but not before (from 22.9 +/- 4.0 to 25.6 +/- 4.5 AU) MCP. Reductions in CO were of the same order before and after MCP. PRA responded to tilt better after than before MCP. Supine PA levels increased with MCP (delta PA = 5.4 +/- 0.7 ng/dl), but its response to tilt was unaltered. There were significant rises in MAP and HR during the cold pressor test after but not before MCP. Our data suggest that vasoconstriction is the main mechanism of MCP improvement in blood pressure response to an orthostatic stimulus in diabetic postural hypotension, possibly because of its antidopaminergic property.

The effect of Collins' solution on the function and structure of isolated proximal convoluted tubules from rabbit kidneys.

Proximal convoluted tubules (PCTs) from rabbit cortical slices were perfused after preservation in Collins' solution with the in vitro microperfusion technique. Under these conditions, after maneuvers of in vitro preservation, the following findings were observed: Tubules were best preserved, functionally and morphologically, when bathed with Collins' solution peritubularly. Tubular preservation was inadequate when the Collins' solution contacted only the luminal or luminal and peritubular sides. These observations indicate a difference in the reactions of various cellular sides to the preservation process, suggesting that during preservation of the whole kidney, there are differences in the preservation of the various tissues of the organ.

Hypertension. A major public health problem in Brazil.

Data collected from various geographical areas show that hypertension is a major public health problem in Brazil. Hypertension is estimated to occur in over 8 million Brazilians and cardiovascular disease-related mortality figures, to which hypertension is a major contributor, increased from 11.8% of the total mortality rate in 1930 to 30.8% in 1980. Costs involved in the treatment of hypertensive patients are very high since hypertension was among the 3 most frequent clinical diagnoses in outpatient visits in 1985. Hypertension is also a major cause of temporary or permanent work incapacitation among Brazilians and data from São Paulo show that hypertension is very common among workers. Finally, demographic tendencies in São Paulo indicate that older age groups have increased in the general population during the past 2 decades. These data, when taken altogether, indicate that hypertension is a major public health problem in Brazil.