Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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 relative role of beta 1- and beta 2-adrenoceptors in the regulation of blood pressure and plasma renin at rest and during exercise was studied in 17 normal male volunteers. They performed, in a randomized order and according to a double-blind crossover study design, three graded and uninterrupted exercise tests until exhaustion after being pretreated during 3 consecutive days with a placebo, with a predominantly beta 1-blocker (atenolol, 50 mg once/day), or with a predominantly beta 2-blocker (ICI 118551, 20 mg 3 times/day). Both drugs caused a decrease of heart rate, but the reduction by ICI 118551 was less pronounced at rest and no additional decline occurred at exercise. ICI 118551 did not affect blood pressure at rest, but during exercise diastolic blood pressure was higher than after a placebo. Atenolol lowered systolic blood pressure at rest and suppressed the exercise-induced increase in systolic blood pressure. At rest and during exercise plasma renin activity was lowered by predominantly beta 1-blockade and unchanged during beta 2-antagonism. The exercise-induced increase in plasma renin was, however, not affected by the beta 1-blocker. After atenolol the urinary excretion of aldosterone was decreased but the plasma aldosterone concentration was not changed. ICI 118551 did not alter plasma or urinary aldosterone. Our results therefore provide further evidence that the adrenoceptors mediating the release of renin at rest and during exercise in humans are partially of the beta 1-subtype, whereas beta 2-adrenergic receptors probably play only a minor role in the control of renin secretion, especially at exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beta-adrenoceptors and the regulation of blood pressure and plasma renin during exercise. 300 20

We compared the antihypertensive efficacy of atenolol (100 mg/d), canrenoate potassium (200 mg/d), and captopril (75 mg/d) in 30 essential hypertensives. The three drugs were administered in a randomized change-over sequence for four-months each. The main variables associated with blood pressure regulation were measured in the basal condition and at the end of each treatment period. The erythrocyte Na transport systems were measured only in the basal condition and at the end of the first treatment period. The average blood pressure reduction was similar for each drug. Mean blood pressure levels after captopril correlated positively with those after atenolol in the individual patients (P less than 0.0001); mean blood pressure levels after canrenoate potassium, on the contrary, did not correlate with those after the other two drugs. Captopril and canrenoate potassium treatment reduced intraerythrocyte Na content (P less than 0.02), canrenoate potassium increased Na-K pump (P0.05), atenolol did not change any erythrocyte membrane Na transport parameters. The ouabain-resistant Na transport systems were not modified by any drug. The patients were divided in three groups according to their antihypertensive response: nonresponders (six patients), canrenoate potassium responders (nine patients) and captopril-atenolol responders (15 patients, equally responsive to both drugs). Nonresponders had the lowest basal Na pump (P less than 0.02). Canrenoate potassium responders had higher basal Na-K cotransport than captopril-atenolol responders (P less than 0.02). Atenolol-captopril responders had the highest basal plasma renin activity (PRA, P less than 0.02). The blood pressure reduction after atenolol correlated with the induced fall in PRA (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antihypertensive effect of captopril, canrenoate potassium, and atenolol. Relations with red blood cell sodium transport and renin. 306 86

The purpose of the present study was to examine the effects of lesions of the nucleus tractus solitarii on the reflex control of sympathetic activity and renin release in the conscious rat. Two doses of the arteriolar vasodilator hydralazine (0.3 and 1 mg/kg, i.v.) were used to activate reflexively the sympathetic nervous system in nucleus tractus solitarii lesion and control rats. Administration of 1 mg/kg of hydralazine to the control rats caused mean arterial pressure to fall from 120 +/- 2 mm Hg to 84 +/- 2 mm Hg and elicited an 11.2-fold increase in plasma renin activity and a 2.7-fold increase in plasma norepinephrine concentration. Administration of 0.3 mg/kg of hydralazine caused the arterial pressure of the lesion group to fall from 118 +/- 3 mm Hg to a comparable value of 85 +/- 4 mmg Hg, but plasma renin activity and plasma norepinephrine concentration did not rise significantly. However, administration of 1 mg/kg of hydralazine to the lesion group caused arterial pressure to fall from 128 +/- 6 mm Hg to 64 +/- 2 mm Hg, in association with a 12.4-fold increase in plasma renin activity and a 1.6-fold elevation in plasma norepinephrine concentration. Atenolol, a beta 1-adrenoceptor antagonist, blocked 70% of the rise in plasma renin activity caused by 1 mg/kg of hydralazine in both groups of rats. In addition, prior renal denervation also markedly attenuated the rise in plasma renin activity caused by hydralazine in the lesion group. Finally, electrical stimulation of the vagus nerves, which caused a large vasodepressor response in the control group, failed to lower the arterial pressure of the lesion group. Based on these observations, we conclude that in the conscious rat (1) nucleus tractus solitarii lesions eliminate the arterial baroreflexes as well as the cardiopulmonary baroreflex, and (2) severe hypotension induces sympathetically mediated renin release in the apparent absence of arterial and cardiopulmonary baroreflex function.
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PMID:Changes in plasma catecholamines and plasma renin activity during hypotension in conscious rats with lesions of the nucleus tractus solitarii. 328 90

Electrolytic lesions of the parabrachial nucleus (PBN) caused significant increases in basal plasma renin activity (+433%) and basal plasma norepinephrine concentration (+98%) in conscious rats. Plasma epinephrine concentration, mean arterial pressure, heart rate, hematocrit, plasma osmolality and plasma sodium and potassium concentrations were not significantly affected by the lesions. Atenolol reduced the elevated plasma renin activity in the lesion group to a value similar to that of a control group (sham lesions or lesions in areas adjacent to the PBN). Captopril significantly lowered mean arterial pressure in the lesion group, but it had no effect on arterial pressure in the control group. Lesions of the PBN also increased the baroreflex-mediated bradycardia evoked by an abrupt elevation of arterial pressure. We propose that the PBN tonically inhibits sympathetic activity, sympathetically mediated renin release and baroreflex sensitivity.
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PMID:Parabrachial lesions increase plasma norepinephrine concentration, plasma renin activity and enhance baroreflex sensitivity in the conscious rat. 331 38

In a double-blind randomised cross-over study atenolol 100 mg daily and matching placebo were given to 14 patients whose blood pressure (BP) was uncontrolled on a fixed dose of captopril and frusemide. Atenolol produced a further reduction in both supine (170/105 mmHg to 163/94 mmHg) and standing (171/114 mmHg to 160/96 mmHg) BP and a significant fall in pulse rate and plasma renin activity (PRA). This fall in BP showed a highly significant correlation with pre-treatment plasma renin levels. No adverse side effects were encountered during the study. Previous suggestions that beta-blockade had no additional hypotensive effect in patients receiving captopril were not substantiated. For patients whose BP was poorly controlled with captopril and a diuretic, a selective beta-blocker is suggested as a useful third line agent.
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PMID:Atenolol improves blood pressure control in patients taking captopril and frusemide. 333 24

Short-term treatment with 1-(p-carbamoyl-methylphenoxy)-3-isopropylamino)-2-propanol (atenolol, Tenormin) (100 mg/d for 5 days) was conducted in 12 patients with labile essential hypertension. Before and at the end of the treatment, cardiohemodynamics, renal hemodynamic and excretory function, and renal pressor (renin-angiotensin-aldosterone) and depressor (renal kallikrein-kinin and prostaglandin) systems were examined. Atenolol decreased cardiac output (CO) without affecting total peripheral resistance. Atenolol also decreased plasma renin activity, plasma aldosterone concentration, urinary excretion of kallikrein-kinin, and urinary excretion of potassium whereas it increased plasma potassium concentration. Urinary excretion of prostaglandin E and sodium was not affected by atenolol. Glomerular filtration rate decreased, but renal plasma flow remained unchanged during the treatment by atenolol. A significant positive correlation was found between the changes in CO and in systolic blood pressure (SBP) while negative correlation was observed between the changes in total peripheral resistance and in SBP. A significant positive correlation was also noted between urinary kallikrein excretion and renal plasma flow. The change in urinary kinin excretion was conversely correlated to that in SBP. This study demonstrates that the hypotensive mechanism of atenolol is very complex. Decrease in CO and inhibition of renin-angiotensin-aldosterone system may mainly be responsible for hypotension. It is likely that potassium retaining action of atenolol partly contributes to its hypotensive action. It is also hypothetized that renal kallikrein-kinin system may play a role in modulating the hypotensive action of atenolol.
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PMID:Mechanism of antihypertensive effect of atenolol in patients with borderline hypertension during short-term treatment. A comprehensive study. 373 23

The interaction of inhibition of prostaglandin (PG) synthesis by indomethacin (75 mg/day) with the antihypertensive effect of atenolol (50 mg b.i.d.) was studied in 11 untreated otherwise healthy men 35 to 45 years old with essential hypertension. Atenolol for 3 weeks decreased supine blood pressure (BP) from 157/109 mm Hg during placebo to 148/97 mm Hg. Indomethacin alone for 1 week slightly increased BP and antagonized the antihypertensive action of atenolol. Atenolol reduced plasma renin activity (PRA) to 40% but did not modify either the urinary excretion of vasodilatory PGs (PGE2 and prostacyclin measured as 6-keto-PGF1 alpha) or plasma kininogen and urine kallikrein. Indomethacin suppressed PRA to 27% and PG excretion to approximately 70% but did not markedly change plasma kininogen and urine kallikrein excretion. The decreased excretion of 6-keto-PGF1 alpha, the metabolite of the main vasodilatory prostanoid prostacyclin, correlated with the increased BP measured in standing subjects. The effects of indomethacin were practically the same when given with atenolol as when given alone. We conclude that the slight increase in BP by indomethacin in essential hypertension is associated with the reduced production of vasodilatory PGs but not with alterations in activities of the renin-angiotensin or kallikrein-kinin systems.
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PMID:Inhibition of prostaglandin synthesis by indomethacin interacts with the antihypertensive effect of atenolol. 389 59

It is difficult for the physician to choose the therapeutic method and the remedy when a plethora is caused by antihypertensive drugs. Apart from the efficacy in the planning of a life-long treatment the compatibility and the simplicity shall increasingly be taken into consideration, for only thus the best possible therapy discipline is to be achieved. Three components--beta-blockers, diuretic and vasodilator--were systematically--alone and combined--applied. Of 188 patients 44% reacted on a beta-blocker alone, 22% on a diuretic alone, other 15% on the combination of the two as well as further 10% only on the triple combination with an addition of vasodilators. The beta-blocker-monotherapy was more successful in younger patients, frequently with high renin content, and in patients up to 60 years. In older patients, more frequently with low renin content, a diuretic or addition of vasodilators was necessary. The blood pressure before the treatment was, however, not decisive for the success of the therapy. In the remaining 9% the beta-blocker was either contraindicated, or even the triple combination did not decrease the diastolic pressure below the desirable aim of 95 Torr. A scheme of therapy, which is based on a beta-blocker, may besides be further simplified by long-acting substances allowing a single daily dosage. This fact is confirmed in a double comparison of Atenolol and Oxprenolol (slow release) in 13 patients. Apart from the favourable relation of effect and compatibility of the beta-blockers these substances antagonize disadvantageous effects of the diuretics and vasodilators. Moreover, they promise a protection of the heart also in the patient with hypertension, which could not be proved with the antihypertensive therapy performed up to now.
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PMID:[Long-term therapy with beta receptor blockaders]. 611 98

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

Hemodynamic (systemic and regional), metabolic and cardiovascular reflexive variables were measured before and after 4 weeks of beta blockade with atenolol in 10 patients with mild essential hypertension. Atenolol reduced mean arterial pressure, heart rate, cardiac index (all p less than 0.005) and renal vascular resistance (p less than 0.01) and increased total peripheral resistance (p less than 0.005). Glomerular filtration rate and renal blood flow were unchanged; plasma renin activity fell 43%. Reflexive cardioacceleration during the Valsalva maneuver and upright passive tilt was blunted. No changes were observed in circulating fluid volumes. In six patients followed for 1 year, blood pressure and heart rate were maintained at levels similar to those during the first 4 weeks. Atenolol was shown to be an effective oral antihypertensive that has no apparent deleterious hemodynamic effects on the renal and splanchnic circulations.
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PMID:Hemodynamics, biochemical and reflexive changes produced by atenolol in hypertension. 612 14


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