The effect of pindolol on plasma renin activity and blood pressure in hypertensive patients.

1 The effect of pindolol administered to twenty-six patients with hypertension of unknown origin was compared with respect to blood pressure and plasma renin activity change after increase of the dose over a period of 6 weeks. 2 There was no clear correlation between the fall of plasma renin activity, which in some patients was very marked, and the fall in blood pressure. Some patients with a fall in plasma renin activity did not drop their pressure. Conversely, some with a fall of pressure did not drop their plasma renin activity. 3 The addition of hydrochlorothiazide to the pindolol finally caused further lowering of the blood pressure in all but one patient and the plasma renin activity rose in all but two patinets. There was no clear correlation between change in plasma renin activity and the effect on blood pressure.     

Effect of pinacidil on blood pressure,plasma catecholamines and plasma renin activity in essential hypertension

Summary Pinacidil, a new cyanoguanidine derivative, is an antihypertensive agent with arteriolar vasodilating properties, which acts on precapillary resistance vessels. A trial was carried out in 30 patients with essential hypertension WHO I-II. The treatment period was divided into three phases. Hydrochlorothiazide (HCTZ) and amiloride were administered for 4 weeks in Phase 1 and supine and standing blood pressure decreased significantly. During Phase 2 pinacidil was added to HCTZ/amiloride for the following 3 months. A further significant reduction in blood pressure was obtained. In the next period of treatment (Phase 3) patients were divided into two groups. For 1 month Group A (15 patients) received pinacidil alone and Group B (15 patients) received HCTZ/amiloride. Conventional laboratory blood tests in all patients remained unchanged during treatment. Reported side effects during Phase 2 were headache (2 patients), dizziness (3 patients), palpitations (2 patients) and ankle oedema (2 patients). Plasma renin activity was slightly increased at the end both of Phases 1 and 2. Plasma catecholamines were increased but not significantly at the end of Phase 2 as compared to Phase 1. The results indicate that pinacidil is effective in lowering blood pressure in mild to moderate essential hypertension.     

硝苯地平在妊娠高血压疾病患者中的应用效果观察

目的 观察硝苯地平在妊娠高血压疾病患者中的应用效果与安全性.方法 选取2011年5月～2013年3月于本院进行治疗的72例妊娠高血压患者为研究对象,将其随机分为对照组36例和观察组36例,对照组仅给予硫酸镁治疗,观察组在对照组的基础上加用硝苯地平,然后将两组的血压控制总有效率、不良反应发生率与治疗前后的平均动脉压（MAP）、全血高切黏度（ηbH）、全血低切黏度（ηbL）及血浆黏度（ηp）进行对比.结果 观察组的血压控制总有效率高于对照组,MAP、ηnH、ηbL及ηp低于对照组（均P＜0.05）,而两组不良反应发生率差异无统计学意义（P＞0.05）.结论 硝苯地平在妊娠高血压患者中的治疗效果较好,安全性较高,对于血压与血黏度的调整也有较好作用.     

Effect of an angiotensin II analogue upon blood pressure, plasma renin concentration and plasma aldosterone in hypertensive patients

Succinamyl-arg-val-tyr-val-his-pro-phenylglycine acetate (succinamyl1-val5-phenylglycine acetate3-A II), an analogue of angiotensin II, has a pressor effect upon patients suffering from primary and secondary hypertension regardless of prevailing plasma renin concentration. It stimulates the release of aldosterone, whereas plasma renin concentration is not influenced. It is concluded, that this new analogue is, as far as its effect upon blood pressure and release of aldosterone in man is concerned, an agonist of angiotensin II.     

A comparison of the effects of prazosin and hydrallazine on blood pressure,heart rate and plasma renin activity in conscious renal hypertensive dogs

Prazosin, a novel antihypertensive agent, and hydrallazine have been compared in renal hypertensive dogs. I.v. prazosin (0.1 mg/kg) produced greater falls in blood pressure than hydrallazine (1 mg/kg i.v.) but, in contrast to hydrallazine, did not cause any significant alteration in heart rate or plasma renin activity in these animals. When given orally, prazosin (0.1 mg/kg) produced falls in blood pressure equivalent to those observed with i.v. hydrallazine (1 mg/kg) again without significant tachycardia or plasma renin activation.     

Effect of nifedipine on plasma renin,aldosterone and catecholamines in arterial hypertension

Summary Acute sublingual administration of nifedipine 10–20 mg to 13 hypertensive patients caused a rapid decrease in blood pressure (BP) and a concomitant increase in heart rate (HR), plasma noradrenaline (NA) and plasma renin activity (PRA); there was no significant change in plasma adrenaline (A) or aldosterone (ALDO). Basal PRA was the major determinant of the rise in PRA, as a close correlation was present between the basal value and the increase caused by nifedipine (r=0.92, p<0.001). The rise in PRA was also correlated with the plasma concentration of nifedipine after 60 min (r=0.80, p<0.01), but it was not correlated with the decrease in BP, the rise in HR or the increase in NA. Nifedipine 30–60 mg daily for 6 weeks caused a reduction in mean BP from 133 to 113 mmHg (p<0.001). Body weight and serum potassium decreased but no consistent change was noted in NA, PRA, ALDO or 24 h-excretion of catecholamines. A significant correlation was present between the change in NA and that in PRA (r=0.74, p<0.01). The alterations in the various parameters in the acute and chronic studies were not correlated. The findings indicate that different regulatory mechanisms are activated during acute and chronic administration of nifedipine. It is suggested that an initial rise in sympathetic activity gradually decreases during prolonged therapy, but it still remains a determinant of PRA.     

The effect of fenigidin (nifedipine) and verapamil on renin activity, the levels of ionized calcium and aldosterone in the blood plasma and on the hemodynamic indices of rats with spontaneous hypertension

Nifedipine and verapamil (10 mg/kg orally) were found to induce a significant increase of renin activity, a decrease of aldosterone and ionized calcium levels in blood plasma in spontaneously hypertensive rats. A preliminary administration of a hypertonic solution of sodium chloride decreased renin activity, ionized calcium and aldosterone levels that contributed to the enhancement of the hypotensive effect of calcium antagonists. It was established that nifedipine by its effect on the parameters of hemodynamics and the condition of renin-angiotensin system as well as the blood plasma ionized calcium level is superior to verapamil.     

Sequential changes in plasma renin activity and plasma catecholamines in mildly hypertensive patients during acute,furosemide-induced body-fluid loss

Summary To evaluate the role of adrenergic mechanisms in the acute response of renin to furosemide, plasma renin activity (PRA) and plasma catecholamine concentrations were measured for 3 h after i.v. administration of furosemide 1 mg/kg to 8 patients with mild essential hypertension. Furosemide induced a prompt and long-lasting increase in renin, with PRA more than doubled at all times. The increase in PRA within the first 30 min paralleled the peak increases in urinary water and sodium flow rates, and significant decreases in plasma volume and central venous pressure. There was no change in plasma catecholamine concentrations. Plasma noradrenaline was increased significantly at 60 min and adrenaline at 90 min, once furosemide had induced a marked loss of body-fluid and 65% decrease in central venous pressure. Both catecholamines remained elevated until the end of the study, whereas urinary water and sodium flow rates had returned to their pre-treatment values by 150 min. Mean blood pressure was essentially unchanged throughout the study, whereas heart rate increased significantly after 90 min. The findings suggest that in mildly hypertensive patients adrenergic mechanisms are not involved in the initial renin response to furosemide, but they come into play later, probably as a result of reflex sympathetic activation triggered by marked volume depletion.     

The relationship of plasma levels of pindolol in hypertensive patients to effects on blood pressure, plasma renin and plasma noradrenaline levels

1. Fifteen, previously untreated, hypertensive patients were given 20 mg of pindolol, orally. The systolic and diastolic blood pressures fell significantly in 1 h; the effect was maximal 4 h after pindolol, and persisted for at least 8 h. 2. After oral administration of 20 mg of pindolol, its concentration in the plasma reached a peak in 2-3 h. At the end of 8 h, pindolol was not detectable in the plasma. 3. There was a significant relationship between the peak concentration of pindolol in plasma and the maximal change in blood pressure in fifteen previously untreated hypertensive patients. In a separate study of nine-nine hypertensive outpatients taking 15-80 mg of pindolol daily, the blood pressure responses corresponded generally to the concentration of pindolol in plasma 2-3 h after the morning dose. 4. There were no significant changes in plasma renin activity, plasma renin concentration or plasma noradrenaline concentration in the previously untreated patients taking 20 mg of pindolol. There was no relationship between initial plasma renin or noradrenaline levels and blood pressure responses to pindolol. Nor was there any significant relationship between the changes in plasma renin or noradrenaline levels and the changes in blood pressure.     

Effect of isoproterenol on blood pressure, plasma renin activity, and water intake in rats

The effects of s.c. administered isoproterenol on blood pressure, plasma renin activity and water intake were studied in unanaesthetized rats as a function of both concentration and time. Isoproterenol (1, 10, 100 and 500 μg/kg) induced a rapid, dose-related decrease in blood pressure and increase in plasma renin activity. Both parameters were found to be nearly normal after 60 min, except after the highest dose. Isoproterenol (? 10 μg/kg) caused a dose-dependent increase in water intake; after the highest dose 5–6 mlH₂O/100 g b.w. was ingested within 60 min. In rats on a sodium-deficient diet, the effect of isoproterenol on renin release and water intake was potentiated whereas in DOCA-pretreated rats, the effect was inhibited. The different actions of isoproterenol, 100 μg/kg were blocked by propranolol, partly (0.5 mg/kg) or completely (2.5 and 10 mg/kg). The results indicate that the action of isoproterenol on water intake is correlated with its ability to induce renin release.     

Time course of blood pressure,pulse rate,plasma renin and metoprolol during treatment of hypertensive patients

Summary Eleven patients were treated for essential hypertension with metoprolol (Selokén^®) for more than three months. The time course of changes in blood pressure, pulse rate and plasma renin activity was studied during treatment with an oral maintenance dose of 100 mg twice daily. Significant decreases in pulse rate, diastolic blood pressure and plasma renin activity were observed even after the first dose. The plasma concentration of metoprolol reached equilibrium after the second dose. After the third dose there was no further significant change in blood pressure. There was a significant correlation (p<0.001) between the initial (after three doses) and final (after >90days) effect of metoprolol on blood pressure (r=0.86 and 0.91 for systolic and diastolic blood pressure change, respectively).     

Short-term effects of atenolol and nifedipine on atrial natriuretic peptide, plasma renin activity, and plasma aldosterone in patients with essential hypertension.

The short-term effects of atenolol and nifedipine on plasma levels of atrial natriuretic peptide (ANP), plasma renin activity (PRA), and plasma aldosterone (PA) were studied in two groups of patients with uncomplicated essential hypertension. Urinary catecholamines, and sodium and potassium excretion were also studied. A group of 20 patients with hypertension, after a wash-out period of at least 10 days, was randomly subdivided into two protocol therapy subgroups. One group (six men and four women) received atenolol (100 mg/d), and the other group (six men and four women) received nifedipine (30 mg/d). Circulating plasma levels of ANP, PRA, and PA were determined by radioimmunoassay, and other variables were determined by routine laboratory techniques before therapy and at day 3 and day 7 after the treatment began. Arterial blood pressure and heart rate were monitored during the study. Both drugs reduced arterial blood pressure (P less than .001) significantly. The atenolol therapy decreased heart rate (P less than .001), increased plasma ANP levels and urinary catecholamine excretion, and decreased PRA and circulating PA levels. Nifedipine treatment did not modify plasma ANP values, whereas it increased PRA and PA circulating levels and urinary catecholamine excretion. No differences were shown for urinary volume, urinary sodium, and potassium excretions during the two different treatments. These findings suggest that the increased plasma ANP levels could contribute to the antihypertensive effects of the beta-adrenoreceptor blockers, by a reduction in PRA and PA levels and a vasodilatative effect.(ABSTRACT TRUNCATED AT 250 WORDS)     

Antihypertensive effect of a calcium antagonistic drug: Regression of hypertensive cardiac hypertrophy by nifedipine

The cardiac hypertrophy which develops in models of sustained hypertension in experimental animals cannot be prevented or reversed by all antihypertensive drugs. Clearly, blood pressure is only one of numerous factors which contribute to the development of hypertensive cardiomegaly. The ability of drugs to reduce cardiac hypertrophy depends primarily on their mode of action, rather than on the degree of blood pressure decrease. Vasodilators effectively control high blood pressure but enhance cardiac hypertrophy in rats. In currect experiments, minoxidil lowered blood pressure, but caused increases in heart weight and plasma-renin activity (PRA) in spontaneously hypertensive rats (SHR). In contrast, the calcium antagonist, nifedipine, reduced blood pressure or prevented its increase in SHR concurrently reducing heart wight and decreasing PRA. Moreever, nifedipine prevented salt-induced hypertension and heart hypertrophy in SD (sensitive)-Dahl rats. It is suggested that in contrast to the vasodilator minoxidil, nifedipine reduces the high renovascular resistance in hypertensives thus enhancing sodium and water elimination. Thus, the action of the calcium antagonist, nifedipine, involve both renal vasodilation and reduction of renin-angiotensin mediated renal vasoconstriction. In this way, the decreased volume load together with the decreased arterial afterload will contribute to the prevention or regression of hypertensive cardiac hypertrophy.     

The effect of atrial natriuretic peptide on plasma renin activity,plasma aldosterone,and urinary dopamine in man

Summary The acute natriuretic effect of human atrial natriuretic peptide (ANP) has been well described in man. We have now studied possible hormonal mediators of this effect.We studied six healthy volunteers on two occasions when they received either an infusion of ANP of 1.5 pmol·kg^–1·min^–1 for 30 min followed by 15 pmol·kg^–1·min^–1 for a further 30 min, or matching vehicle infusions in a randomized single-blind fashion.On the placebo day, plasma renin activity (PRA) rose from 1.26±0.08 to 1.57±0.14 ng A1·ml^–1·h^–1, while on the ANP study day PRA fell from 1.45±0.15 to 1.28±0.05 ng A1·ml^–1·h^–1 (p<0.01). No significant changes were found in plasma aldosterone concentrations or in urinary dopamine excretion.These results provide evidence that ANP suppresses renin release in man.     

Effects of swim training alone and in combination with clonidine and rilmenidine on blood pressure, plasma electrolytes, vasopressin, and renin activity in spontaneously hypertensive rats.

Adaptations to the effects of clonidine (CL) and rilmenidine (R) were studied during a 12-week training program (swimming) in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Systolic blood pressure (SBP) was regularly measured during this period. Body weight (BW) was determined at the beginning and at the 12th week. Plasma parameters, cardiac determinations, vasopressin (pAVP), and plasma renin activity (PRA) were measured only at the end of the experiment. Both SBP and ponderal benefit were reduced by CL, R, and training. Contrary to beta-adrenoceptor blocking agents, we found no inhibition of the beneficial effect on SBP of training in combination with CL or R. Plasma and hypothalamic vasopressin were reduced by both drugs but only CL increased plasma renin activity (PRA) although its mechanisms of action are still not clearly understood. Our results suggest that CL and R as well as swim training can be considered as an effective countermeasure in SHR. Moreover, the heterogeneity of action of CL and R on some of the parameters tested is in favor of different pharmacological properties for these drugs.