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)

Intrarenal adenosine concentration is threefold greater in the one-kidney, one clip hypertensive rat compared with normotensive animals. Since exogenously administered adenosine may increase renal blood flow by direct vasodilation, inhibition of renin release, or prejunctional interruption of adrenergic neurotransmission, these studies examined whether endogenous intrarenal adenosine maintains renal blood flow distal to renal arterial stenosis. Administration of theophylline, which blocks the direct vasodilating effect of adenosine and antagonizes the inhibitory effect of adenosine on renin release and sympathetic neurotransmission, resulted in marked renal vasoconstriction in one-kidney, one clip hypertensive animals. This theophylline-induced renal vasoconstriction was markedly attenuated by angiotensin II blockade with saralasin and was unchanged by renal denervation or beta 1-adrenergic blockade with atenolol. These findings indicate that the marked renal vasoconstriction in one-kidney, one clip hypertension during theophylline administration is mainly mediated by angiotensin II, is to a lesser degree due to inhibition of adenosine-induced vasodilation, and is independent of sympathetic influences. These data suggest that endogenous interstitial adenosine preserves renal blood flow in one-kidney, one clip hypertension mainly by inhibiting renin release.
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PMID:Endogenous intrarenal adenosine preserves renal blood flow in one-kidney, one clip rats. 339 75

To determine whether the increase in renin secretion rate (RSR) produced by the beta 2-adrenoceptor agonist epinephrine was dependent on intact renal innervation, epinephrine (10 ng X kg-1 X min-1) was infused bilaterally into an innervated and a denervated kidney (ira) of the same anesthetized dog at spontaneous and reduced renal arterial pressure (decreases RAP, 100 mmHg). Epinephrine ira did not affect mean arterial pressure, renal hemodynamics, or urinary sodium excretion of either kidney. At spontaneous RAP epinephrine ira increased RSR from 633 +/- 134 to 926 +/- 137 ng/min in innervated kidneys but did not change RSR in denervated kidneys. decreases RAP in the presence of epinephrine ira resulted in an increase in RSR from 969 +/- 248 to 2,564 +/- 630 ng/min in innervated kidneys, which was greater than that produced in the absence of epinephrine, from 741 +/- 244 to 1,606 +/- 431 ng/min. In denervated kidneys decreases RAP resulted in similar increases in RSR in the absence and presence of epinephrine ira from 41 +/- 15 to 166 +/- 60 ng/min and from 59 +/- 210 to 235 +/- 78 ng/min, respectively. These results demonstrate that the increase in RSR produced by epinephrine is dependent on intact renal innervation at spontaneous and decreases RAP and suggest that epinephrine increases RSR by a prejunctional mechanism. The beta 1-adrenoceptor antagonist metoprolol (0.3-0.5 microgram X kg-1 X min-1 ira) abolished the enhanced RSR response to decreases RAP produced by epinephrine ira. Similarly, the beta 2-adrenoceptor antagonist ICI 118551 (0.005-0.25 microgram X kg-1 X min-1 ira) abolished the enhanced RSR response to decreases RAP produced by epinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interaction between epinephrine and renal nerves in control of renin secretion rate. 352 29

In congestive heart failure (CHF) both the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone-system (RAAS) are activated. Both phenomena are only of short-term benefit and inevitably detrimental with prolonged activation. There are many possibilities for interaction between the systems, in particular when they are both in the activated state as in CHF. Renin release from the renal juxtaglomerular cells is stimulated by the SNS via beta 1-adrenoceptors. At a higher level of renal nerve stimulation there is recruitment of antinatriuretic and finally vasoconstrictor activity, mediated by alpha 1-adrenoceptors. The vasoconstrictor potency of angiotensin II (AII) involves both postsynaptic angiotensin II-receptors and also various processes stimulating sympathetic activity and its sequelae. The following sympathetic components may contribute to the effect of angiotensin II:ganglionic stimulation; enhanced release of noradrenaline (tyramine-like effect); inhibited noradrenaline re-uptake; facilitation of noradrenaline release via presynaptic AII-receptors; sensitization of postsynaptic alpha-adrenoceptors. The presynaptic AII-mechanism is probably the most sensitive and relevant process, which is also involved in the vasodilator activity of ACE-inhibitors.
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PMID:Interaction between the adrenergic and renin-angiotensin-aldosterone-systems. 353 60

The very diverse clinical expressions of pheochromocytoma are dependent upon type of catecholamine secreted and excreted by the tumor. The role of each of the three amines (adrenaline, noradrenaline, dopamine) is reviewed in relation to physiologic regulation of blood pressure: adrenaline and noradrenaline are pressor hormones and act on almost all blood pressure factors. They possess chronotropic and positive inotropic effects by their action on cardiac beta 1 adrenoceptors, a peripheral vasoconstricting action by interaction with vascular alpha 1 receptors and a direct effect on renin production and tubular resorption of sodium. Inversely, dopamine presents as a hypotensive agent, opposing effects of adrenaline and noradrenaline and possessing numerous sites of action: central hypotensive action on cardiovascular integration structures, inhibitory effect on sympathetic ganglionic neurotransmission, action on specific presynaptic receptors at nerve endings, reducing sympathetic vasoconstrictor tone and finally a direct vasodilator effect. Based on these recent physiologic data the role is discussed of hypersecretion of each amine in the cardiovascular expression of pheochromocytoma. Attention should be concentrated on the nature of hormonal hypersecretion of pheochromocytoma, and a determining role given to the type of catecholamine secreted by the tumor and to the relation between the different amines with respect to the blood pressure symptomatology of pheochromocytoma.
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PMID:[Catecholamines in the cardiovascular expression of pheochromocytomas. I. Physiological role of noradrenaline, adrenaline and dopamine]. 353 37

The effects of labetalol on the secretion of prostacyclin and plasma-renin activity (PRA) were evaluated, relative to a control group in 24 patients undergoing hip osteotomy. They were randomly assigned to two groups (G-I and G-II) with 12 patients each. Patients allocated to both groups received standard anaesthesia (thiopentone, pancuronium, fentanyl and nitrous oxide). Patients belonging to Group II were given labetalol at a dose of 0.8 mg kg-1. The stable metabolite of PGI2, 6-keto-PGF1 alpha was quantified from urine samples by radioimmunoassay (RIA). Cortisol, PRA and aldosterone were determined from blood samples. A significant increase in 6-keto-PGF1 alpha elimination was observed in G-I. Labetalol administration partially but significantly inhibited this increase. We believe that prostacyclin is involved not through the beta 1 but through the alpha 1 receptors in the secretion of renin.
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PMID:The effect of labetalol on urinary prostacyclin secretion during surgery. 353 90

The pathogenesis of hypertension accompanying diabetes mellitus (DM) may involve abnormalities in at least two major blood pressure (BP)--regulating systems. Exchangeable sodium (Naex) and the cardiovascular pressor responsiveness to norepinephrine are often increased, while blood volume is normal or low, regardless of age, insulin-dependence or non-dependence, or the presence or absence of retinopathy or clinical nephropathy. In hypertensive DM, systolic BP correlated (P less than 0.001) with Naex; diuretic treatment improved norepinephrine responsiveness, Naex and BP, while calcium entry blockade improved cardiovascular responsiveness and BP without changing Naex. Plasma catecholamine, renin and aldosterone levels are usually normal or sometimes low in stable DM. Antihypertensive therapy in DM is based on 3 legs, namely antidiabetic treatment, general measured aimed at reducing BP and associated risk correlates, and if necessary BP-lowering drugs. Due to their metabolic side effects, thiazide-diuretics given in moderate to high doses are not ideal step 1 drugs in DM. Certain beta 1-blockers have fewer, although still some, unwanted side effects. Preliminary data suggest that certain calcium antagonists may often lower BP without causing relevant metabolic impairment. These agents and converting enzyme inhibitors deserve further evaluation in the treatment of DM-associated hypertension.
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PMID:Pathogenesis and treatment of hypertension associated with diabetes. 386 82

The initial antifailure efficacy of beta-adrenergic agonists is generally lost during prolonged treatment. The reasons are not fully understood. In 11 patients with advanced cardiac decompensation due to dilated cardiomyopathy, prenalterol, a selective beta 1 adrenergic agonist, improved the left ventricular contractility after acute intravenous and during prolonged oral administration. However, after periods of treatment ranging from 2 to 18 weeks, blood pressure and systemic vascular resistance were raised in each patient. These changes resulted in an increase of the left ventricular afterload which was such as to overwhelm the effects of the enhanced contractility, and to extinguish the initial improvement of the cardiac function and of the clinical condition. Stimulation of the presynaptical beta-receptors facilitating norepinephrine release or of the renin secretion by this beta 1 agonist, may be the causes of the systemic vasoconstriction and of the loss of effectiveness in the long run.
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PMID:Hemodynamic response to oral prenalterol in dilated decompensated cardiomyopathy as a result of cardiac and vascular effects. 408 67

The efficacy and tolerability of the new ACE-inhibitor enalapril (MK 421) and the beta 1-selective adrenoceptor blocker atenolol for the treatment of primary hypertension were compared in a double blind parallel study. 12 patients were randomized to each drug. The doses of enalapril were 20 and 40 mg o.d. and of atenolol 50 and 100 mg o.d. for 4 weeks each, whereafter hydrochlorothiazide (HCTZ) 25 or 50 mg o.d. was added if necessary to achieve a supine diastolic blood pressure (BP) less than 90 mm Hg 24 hours after drug intake. Supine BP was reduced from 160 +/- 7/111 +/- 4 mm Hg to 153 +/- 13/101 +/- 9 mm Hg (p less than 0.05/p less than 0.005) with enalapril and from 163 +/- 17/109 +/- 6 mm Hg to 145 +/- 11/95 +/- 7 mm Hg (p less than 0.005/p less than 0.001) with atenolol. The addition of HCTZ caused a profound additive BP reduction to 132 +/- 7/88 +/- 6 mm Hg with enalapril and to 130 +/- 10/88 +/- 7 mm Hg with atenolol. There was no significant difference between the efficacy of enalapril and atenolol alone or combined with HTCZ. The reduction in mean arterial pressure with enalapril tended to correlate with pre-treatment stimulated plasma renin activity and 24 hours urinary kallikrein excretion. Both drugs tended to reduce serum and urinary aldosterone and kallikrein excretion to the same extent. There was one drop-out in each group, one due to impotence on the combination of enalapril and HCTZ and one due to peripheral coldness during atenolol treatment. Other side effects were mild. No toxic adverse effects were registered.
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PMID:Enalapril and atenolol in primary hypertension--a comparative study of blood pressure lowering and hormonal effects. 608 25

The albuminuria occurring after swimming in splenectomized dogs was investigated. Swimming in splenectomized dogs induces metabolic acidosis, a decrease in renal vascular conductance, and an increase in plasma renin activity, all three factors possibly implicated in the occurrence of albuminuria. The administration of sodium bicarbonate prior to swimming reduced the magnitude of the acidosis and eliminated the increase in albuminuria after swimming. Phenoxybenzamine, an alpha-adrenergic blocking agent that maintains the renal blood flow during exercise also blocked the increase in albuminuria despite a decrease of blood pH during swimming. However, after metoprolol, a beta 1-adrenergic blocking agent that blocks the rise in plasma renin activity during exercise, swimming causes a threefold increase in albuminuria (P less than 0.01). The albuminuric response to swimming preceded by saline was also significant (P less than 0.05). It is likely that post-swimming albuminuria in splenectomized dogs is linked to the decrease of renal vascular conductance or to the decrease in blood pH rather than to the rise in plasma renin activity.
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PMID:Effects of NaHCO3, alpha-, and beta-adrenergic blockade on albuminuria after swimming in splenectomized dogs. 609 80

Since beta-adrenergic blockers are effective in the therapy of hypertension by a mechanism related to the degree of activation of the renin-angiotensin system, the effect of eight beta blockers was examined on angiotensin II potentiation of nerve stimulation (NS) in isolated perfused rat mesenteric vessels. The vasoconstrictor response to periarterial NS was obtained by monitoring changes in perfusion pressure while a beta blocker or a beta blocker and angiotensin II (3 ng/ml) were added to the perfusate. Although each beta blocker tended to decrease responses to NS, in the concentrations used, only metoprolol significantly inhibited responses to NS. Angiotensin II, when infused alone, potentiated the responses to NS by 63% (p less than 0.01). These enhanced responses following angiotensin II were inhibited in a dose-related manner (10--300 ng/ml) by beta 1, beta 2, and mixed beta blockers. At the 100 ng/ml concentration, DL-propranolol, timolol, metoprolol, practolol, butoxamine, and H35/25 inhibited the angiotensin II potentiation of NS by 83%, 76%, 77%, 59%, 72%, and 41% respectively. The order of potency for this action was as follows: timolol = metoprolol = butoxamine greater than propranolol greater than practolol greater than H35/25. Administration of D- and L-propranolol also reduced the responses by 75%. The vasoconstrictor responses to injected norepinephrine (NE), in the presence and absence of angiotensin II, were not altered by DL-propranolol or timolol. In conclusion, beta-adrenergic blockers were found to interfere with the effect of angiotensin II on the sympathetic neuron, a property that could contribute to the antihypertensive action of these drugs.
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PMID:Inhibition of angiotensin II potentiation of sympathetic nerve activity by beta-adrenergic antagonists. 610 65


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