Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distributions of angiotensinogen and specific renin activity were examined in the brains of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto controls (WKY). Specific renin activity was markedly elevated in the pituitary of SHR compared to WKY. Renin levels in other regions of SHR brain were either significantly lower or similar compared to WKY. In contrast, angiotensinogen was significantly elevated in several regions of SHR compared to WKY brain. These results indicate involvement of a brain renin-angiotensin system in the development of genetic hypertension.
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PMID:Regional distribution of renin and angiotensinogen in the brain of normotensive (WKY) and spontaneously hypertensive (SHR) rats. 388 47

A short review of the literature shows hypertension as one of the many possible side effects of oral contraceptives. The hypertension apparently develops as a result of stimulation of the renin-angiotensin-aldosterone system. Studies have demonstrated this action to be attributable to the estrogen component, since progesterone has not shown any laterations of plasma renin levels. The stimulation of the renin-angiotensin-aldosterone system during the luteal phase of menstruation is due to the natriuretic aldosterone-antagonistic effect of progesterone. Various experiments with rats have confirmed these effects. Since almost all women have shown a stimulation of this system after taking ovulation inhibitors, the question is why they all do not develop hypertension. There are some experimental data for the hypothesis that only those women will become hypertensive whose renin secretion due to the effects of raised angiotensin and aldosterone activity has not been damped. From the findings it is clear that a patient on oral contraceptives must have her blood pressure regularly controlled, particularly in cases of preexisting hypertension or familial hypertension. Should high blood pressure or hypertension occur, the drugs must be stopped even if the estrogen-induced hypertension is reversible after cessation of the medication.
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PMID:[Oral contraceptives and hypertension]. 432 89

The preventative effects of betablockers and captopril on the development of genetic hypertension in genetically hypertensive rats, were studied after long-term daily dosage by forced feeding, from the 5th to the 20th week of age of the animals. Of the drugs studied, captopril, atenolol and propranolol limited the development significantly, but pindolol only had a modest effect and acebutolol was ineffective. No correlation was found between the degree of prevention of genetic hypertension and the intensity of betablockade. Atenolol and propranolol prevent genetic hypertension by I) reducing cardiac output, a reduction which is not neutralised by the simultaneous change in peripheral resistance, 2) decreasing plasma renin concentrations, and 3) limiting the development of myocardial hypertrophy. Captopril is very effective in preventing the development of genetic hypertension and acts: 1) by causing an early and lasting fall in peripheral resistance related to the suppression of Angiotensin II, and possibly by potentialising the vasodilatation of bradykinins and, 2) by limiting myocardial hypertrophy.
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PMID:[Comparison of the effects of betablockers and captopril on the development of genetic hypertension in the rat]. 611 62

The relationship between the kidney and genetic hypertension has been assessed in light of the changes seen in some kidney and cell functions during the phases preceding and accompanying the development of "genetic" types of hypertension in rats and humans. Comparison of the kidney function of normotensive subjects likely to develop hypertension with that of matched controls resistant to hypertension showed, in the former, a higher glomerular filtration rate (GFR), greater tubular reabsorption, larger 24-h urinary output, larger fraction of cardiac output to the kidney, and lower plasma renin activity. After the transplantation of a kidney from a subject in the hypertension-prone group, recipients had higher blood pressure and required more antihypertensive therapy than recipients of kidneys from the hypertension-resistant group. In humans this finding is not as clear as in rats. During the development of hypertension most of these differences in kidney function in the two groups of subjects tend to disappear. The changes in cell function, measured particularly in rats, were consistent with the organ function changes. Cell volume and sodium content were lower, while the transport rate across the cell membrane was faster in proximal tubular cells of rats with genetic hypertension than in the appropriate controls. This is in keeping with the concept of a primary increase in proximal tubular reabsorption leading, on the one hand, to an increase in GFR and renal blood flow and a decrease in renin and, on the other, to an increase in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Genetic hypertension and the kidney. 620 36

MK 421, at the dose of 25 mg/kg, administered daily by gavage to spontaneously hypertensive rats (SHRs) from their 4th to 15th weeks of age almost completely inhibited development of genetic hypertension. Since heart rate and cardiac and systolic indexes were not affected by the drug, prevention of genetic hypertension development was solely related to an early, potent and long-lasting reduction of the progressive increase of the peripheral resistance which generally develops in SHRs during ageing. MK 421 reduced body growth but did not modify fluid intake, plasma NA+ and urine volume, thus water and salt retention did not develop. MK 421 enhanced vascular responsiveness to norepinephrine and angiotension II and reduced myocardial hypertrophy. Plasma renin concentration was increased and urinary antidiuretic hormone did not change. Finally, MK 421's preventive effects against genetic hypertension development persisted up to 10 weeks after discontinuation of treatment.
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PMID:MK 421 and prevention of genetic hypertension development in young spontaneously hypertensive rats. 628 98

MK 421, 25 mg/kg, administered daily by gavage to young spontaneously hypertensive rats (SHRs) from their 4th to 15th weeks of age almost completely inhibited genetic hypertension development. Since heart rate and cardiac index were not drug affected, prevention of genetic hypertension development was solely related to an early, potent and long-lasting limitation of the progressive increase in peripheral resistance which normally develops in SHRs during ageing. MK 421 slightly enhanced vascular responsiveness to exogenous norepinephrine and angiotensin II and reduced myocardial hypertrophy. Plasma renin concentration was increased. MK 421 slightly reduced body growth but did not affect fluid intake, urinary volume and urinary ADH, demonstrating that no water or salt retention developed. Finally, MK 421's preventive effects against genetic hypertension development persisted up to 10 weeks after treatment discontinuation.
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PMID:[Prevention of the development of genetic hypertension by MK 421 in the SHR]. 628 57

To clarify the possible risk factors for the development of hypertension, we examined the influences of heredity and environment on blood pressure regulation and whether or not the physiological condition differed in high school students with different levels of blood pressure. A borderline hypertensive (BH) group, consisting of 75 male students with systolic blood pressure (SBP) consistently above 140 mmHg on two separate occasions, was compared to a normotensive (N) group of 84 male students with SBP below 130 mmHg. In the BH group, 43% of students had a family history of hypertension within two generations of relatives, while 18% had one in the N group (p less than 0.05). The BH group was characterized by a gain in weight, a slight increase in 24-hour urinary sodium excretion, a higher heart rate, elevated values of plasma renin and urinary aldosterone, and an elevated sodium concentration in erythrocytes. Nevertheless, urinary excretion of potassium and kallikrein did not differ between the two groups. In each group, students with familial hypertension had a significantly (p less than 0.05) lower 24-hour urinary kallikrein excretion than those without it. Although kallikrein excretion correlated fairly well with aldosterone excretion (r = 0.47, p less than 0.01) or creatinine clearance (r = 0.59, p less than 0.01) in the BH students without familial hypertension, no such correlations were found in those with familial hypertension. These results indicate that the abnormal relationships of aldosterone to kallikrein metabolism and of kallikrein to renal function control may be involved as hereditary factors in the development of hypertension.
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PMID:Environmental and physiological characteristics in adolescents genetically predisposed to hypertension. 633 71

1. The preventive effects against genetic hypertension development (GHD) of seven antihypertensive drugs chronically administered to the young SHRs from their 5th to their 13th week of age have been investigated. 2. While prazosin (20 mg/kg) and hydrochlorothiazide (6,5 and 25 mg/kg) are ineffective and while YC 93, a calcium-antagonist (10, 30, 100 mg/kg) exerts only a slight protective effect, captopril (30 and 100 mg/kg), dihydralazine (25 mg/kg) and atenolol (200 mg/kg) strongly prevent GHD. 3. Captopril and dihydralazine oppose GHD by inhibiting the progressive increase in peripheral resistance (PR) which normally occurs with ageing in SHRs. Simultaneously, these two drugs do not affect the cardiac output (CO) but increase plasma renin concentration (PRC). On the other hand, atenolol opposes GHD mainly by reducing CO and PRC while it simultaneously reinforces the progressive increase of PR with age. Captopril and atenolol, unlike dihydralazine, limit SHRs' myocardial hypertrophy. 4. After 14 weeks of treatment, arterial blood pressure (BP) of dihydralazine - and atenolol-treated animals meets control animals BP within 4 weeks whereas captopril preventive effects are still present up to 12 weeks after treatment discontinuation. Wit atenolol and captopril ther is after treatment discontinuation a good correlation between the evolution of heart weight/body weight and BP, which suggests that captopril could temporarily oppose the myocardial structural alterations which usually accompany GHD.
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PMID:[Antihypertensives and the prevention of development of genetic hypertension in the hypertensive SHR rat]. 646 Feb 15

The effects of propranolol (100 mg/kg), atenolol (200 mg/kg) and acebutolol (1000 mg/kg) administered daily by gavage to spontaneously hypertensive rats (SHRs) from their 6th to 20th weeks of age were investigated on genetic hypertension development (GHD) and at regular intervals on heart rate (HR), cardiac output (CO), stroke volume (SV), peripheral resistence (PR), plasma renin concentration (PRC) and heart weight/body weight ratio (HW/BW). Treatment with propranolol and especially atenolol markedly inhibited GHD while acebutolol was ineffective. No correlation was found between GHD prevention and (1) the degree of beta-adrenergic blockade (2) the reductions in HR and CO and (3) the decrease in PRC induced by the three treatments. Although none of the three drugs prevented the progressive increase in PR which develops in SHRs during their growth, propranolol and atenolol opposed GHD mainly by reducing CO, this effect being however partly counterbalanced for atenolol by a secondary potentiation of PR increase. With acebutolol, a similar reinforcement of PR increase occurred which completely neutralized the reduction in CO, resulting in the drug's ineffectiveness against GHD. These differential effects of the three drugs probably reflect different early induced structural modifications at cardiac and/or vascular levels.
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PMID:beta-Adrenoreceptor blockage and genetic hypertension development in rats. 699 80

Captopril (100mg/kg) administered daily by gavage to young spontaneously hypertensive rats (SHRs) from their 6th to 20th weeks of age almost completely inhibited genetic hypertension development (GHD). This effect was correlated with an early and long-lasting limitation of the progressive increase in peripheral resistance which normally develops in SHRs during their growth. Heart rate, cardiac and systolic indexes remained unchanged, plasma renin concentration was significantly increased and heart weight/body weight ratio was significantly decreased. At last, captopril's GHD preventive effect persisted up to 12 weeks after treatment discontinuation.
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PMID:Captopril and hypertension development in the SHR. 700 5


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