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

Forskolin, a novel receptor-independent adenylate cyclase activator, stimulated renin release from the isolated perfused rat kidney twofold at 10(-7) M and threefold at 10(-6) M. This stimulation was blocked by angiotensin II but not by the beta-adrenoceptor antagonist atenolol. These findings strengthen the concept that an intracellular increase of 3',5'-cyclic AMP by adenylate cyclase activation can induce stimulation of renin release.
 ...
PMID:Forskolin stimulates renin release from the isolated perfused rat kidney. 612 35

To assess the effects of nitroglycerin ointment (NTG) on hemodynamics and autonomic nervous activity, 17 normal subjects and 13 patients with severe congestive heart failure (CHF) were studied. In 12 normal subjects, NTG significantly increased the plasma norepinephrine concentration in association with a slight reduction in systolic blood pressure and a slight increase in heart rate, plasma cyclic adenosine monophosphate (cyclic AMP) concentration, and renin activity at 1 hr. All normal subjects complained of headache or felt heavy-headed after NTG administration. In the 13 patients with CHF, NTG significantly decreased plasma norepinephrine and cyclic AMP concentrations in association with a significant increase in the cardiac index and a significant reduction in pulmonary arterial diastolic pressure, systemic vascular resistance, systolic blood pressure, and heart rate. The effects occurred at 30 min after NTG administration and continued for 3 hr. Relief from dyspnea or orthopnea in patients with CHF was observed. NTG did not change the plasma cyclic GMP concentration in normal subjects and patients with CHF. We conclude that in patients with CHF, NTG decreases the enhanced sympathetic nervous activity, with concomitant beneficial effects on hemodynamics and improvement of clinical symptoms. In contrast, NTG increases sympathetic nervous activity in normal subjects.
 ...
PMID:Effects of nitroglycerin ointment on plasma norepinephrine and cyclic nucleotides in congestive heart failure. 616 16

These experiments were designed to elucidate which of two second messengers (cyclic 3',5' adenosine monophosphate [c-AMP]; intracellular calcium [Cai]) was more closely related to the renin secretory process. The rat renal cortical slice preparation was used. Agents which previously were shown to inhibit basal renin secretion by increasing Cai (ouabain, vanadate, angiotensin II, antidiuretic hormone, and 60 mM K) antagonized and/or blocked isoproterenol-stimulated secretion, which is thought to be mediated by adenylate cyclase activation and increased levels of c-AMP. The stimulatory effect of dibutyryl c-AMP was antagonized and/or blocked by the same agents which antagonized and/or blocked isoproterenol-stimulated secretion. Thus, the inhibitory effects of these agents on isoproterenol-stimulated secretion cannot be explained by a Ca-induced decrease in c-AMP production. Secretory rate was stimulated by a potent phosphodiesterase inhibitor (3-isobutyl-1-methylxanthine). A combination of this and dibutyryl c-AMP produced even greater stimulation. Ouabain blocked the stimulatory effect of this combination. These results are not consistent with an invariant direct relationship between c-AMP and renin secretory rate, but are consistent with an inverse relationship between Ca; and renin secretion. Further, they are consistent with the hypothesis that in isoproterenol-stimulated renin secretion. c-AMP is the second and Cai the third or the final messenger.
 ...
PMID:Isoproterenol-stimulated renin secretion in the rat: second messenger roles of Ca and cyclic AMP. 617 94

In order to determine the molecular basis for the loss of catecholamine responsiveness in skeletal muscle in chronic azotemia, plasma and serum levels of catecholamines and other hormones whose mechanisms of action are associated in part with cyclic nucleotide mediation were assessed in 37 patients with chronic azotemia. Samples were obtained prior to and immediately following conventional hemodialysis. Plasma epinephrine and norepinephrine levels in patients predialysis were increased 50% and 25% respectively compared to control subjects. Levels of insulin, prolactin, aldosterone and renin were also in creased in azotemic patients prior to dialysis. Conventional hemodialysis reduced serum levels of growth hormone, but had no effect of the elevated levels of all other hormones found in patients predialysis. In particular, plasma epinephrine and norepinephrine levels were unaffected by hemodialysis. Despite these findings, hemodialysis did reduce to normal levels the elevated plasma levels of cyclic AMP and cyclic GMP observed in uremic subjects predialysis. These data are consistent with increased adrenergic outflow in patients with chronic azotemia, and suggest a mechanism of homologous desensitization of the catecholamine receptor adenylyl cyclase unit in chronic azotemia.
 ...
PMID:The effect of hemodialysis on levels of cyclic nucleotide-associated hormones in patients with chronic renal failure. 625 22

Cyclic AMP (cAMP) is the intracellular mediator of beta-adrenergic stimulation in most tissues. Stimulation of beta-adrenoceptors increases renin release much more at low than at control arterial perfusion pressure. If beta-adrenergic stimulation is mediated by cAMP, this nucleotide should also potentiate renin release at low perfusion pressure. In anaesthetized, propranolol treated dogs, the dibutyryl derivative of cAMP (DB-cAMP), which penetrates cell membranes more readily than cAMP, increased renin release significantly during renal arterial constriction at a perfusion pressure below the range of autoregulation, but no significant effect was observed at control blood pressure. A dose-response relationship could be demonstrated in propranolol treated dogs by administering DB-cAMP at 10, 100 and 1000 micrograms/min at low but not at control blood pressure. Since sodium excretion increased, stimulation of a macula densa mechanism is unlikely, whereas arteriolar dilation, caused by autoregulation at low blood pressure, may condition the juxtaglomerular apparatus for renin release. Infusion of cAMP had no effect on renin release either at control or low blood pressure, whereas 5'AMP exerted a marked inhibitory effect at low blood pressure. We conclude that infusion of DB-cAMP rather than cAMP stimulates renin release at low but not at control blood pressure and that this effect is not mediated by beta-adrenergic receptors; cAMP may be an intracellular mediator of renin release.
 ...
PMID:Conditions for stimulation of renin release by cyclic AMP in anaesthetized dogs. 627 77

Isoproterenol, dopamine, glucagon and dibutyryl cyclic AMP (DB-cAMP) increase renin release at low but not at control blood pressure. These findings suggest that autoregulated afferent arteriolar dilation is a prerequisite of renin release mediated by intracellular generation of cyclic AMP. To examine this hypothesis further the effects on renin release of theophylline, which would maintain high intracellular concentration of cAMP by inhibiting phosphodiesterase, were studied in anesthetized dogs. After inhibiting beta-adrenergic stimulation with propranolol, theophylline increased renin release significantly from 0.7 +/- 0.2 to 1.8 +/- 0.7 micrograms/min at control blood pressure and from 23 +/- 4 to 41 +/- 5 micrograms/min at a renal perfusion pressure of about 50 mmHg. The greater effect at low blood pressure occurred despite adjustment of the infusion rate of theophylline to keep arterial plasma concentration of theophylline unaltered. Isoproterenol infusion at low blood pressure raised renin release from 41 +/- 11 to 76 +/- 19 micrograms/min before and 54 +/- 13 to 108 +/- 31 micrograms/min during continuous infusion of theophylline. The renin release response to infusion of theophylline at low blood pressure was not enhanced by DB-cAMP infusion. We conclude that arteriolar dilation provides a condition for stimulation of renin release during the theophylline infusion. Theophylline infusion may augment the effect of isoproterenol on renin release by delaying the intracellular degradation of cAMP.
 ...
PMID:Conditions for augmentation of renin release by theophylline. 631 54

These studies were undertaken to clarify the role of the central and peripheral sympathetic nervous system and the renin-aldosterone system on the onset and maintenance of high blood pressure in essential hypertension (EH), and the following examinations were performed: 1) Urinary free norepinephrine and epinephrine excretion (UNEf and UEf), urinary conjugated norepinephrine and epinephrine excretion (UNEconj and UEconj), plasma norepinephrine and epinephrine concentration (PNE and PE), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were measured in 52 patients with EH, who were divided into two groups (borderline EH: b-EH, and sustained EH: s-EH), and fifteen normals (N). 2) Cardiac index (CI), total peripheral resistance index (TPRI), appearance time, mean transit time and stroke index (SI) were determined by the dye-dilution method in eight patients with b-EH, ten patients with s-EH and ten N. 3) Clonidine was administered orally in a single dose of 150 micrograms to seven patients with s-EH and three patients with b-EH, and PNE, PE and growth hormone (GH) were measured before and after the administration. 4) Isoproterenol was infused intravenously in a dose of 0.02 microgram/kg/min for 30 min to 18 patients with s-EH and six N, then plasma cyclic AMP (c-AMP) and PRA were determined before, during and after the infusion. 5) Methacholine was injected intramuscularly in a dose of 10 mg to seven N, and PNE, PE and PRA were measured before and after the injection. There were no significant differences of PNE, PE, UNEf and UEf among the three groups (b-EH, s-EH and N), but UNEconj in both b-EH and s-EH was higher than in N (b-EH: p less than 0.1, s-EH: p less than 0.05). PRA in s-EH was slightly lower not only in N but also in b-EH. PAC in b-EH and s-EH was slightly lower than in N. The difference of PAC between b-EH and s-EH was not found. CI and SI were higher than in N (p less than 0.05), but TPRI was normal. In s-EH, TPRI was slightly elevated as compared with b-EH (p less than 0.1). In s-EH, clonidine caused a significant lowering of both blood pressure and PNE with a simultaneously marked increment of GH; on the other hand, in b-EH blood pressure and PNE did not change significantly in spite of the distinct rise of GH. After the isoproterenol infusion, PRA and c-AMP increased, and there was a significant correlation between the initial level of PRA and the maximal increment of PRA after the infusion in both s-EH and N.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:[Studies on the role of the central and peripheral sympathetic nervous system and the renin-aldosterone system on the onset and maintenance of high blood pressure in essential hypertension]. 632 58

A 53-year-old man with retinitis pigmentosa, who had two years' complaints of general malaise and muscle weakness, noticed occasional attacks of the cramps of the lower legs about three months prior to admission. At that time, hypocalcemia (7.6 mg/dl) and hyperphosphatemia (5.2 mg/dl) were pointed out. On admission, serum potassium was high-normal or high (4.4 - 4.9 mEq/l). Endocrinological studies revealed the findings of pseudohypoparathyroidism (PHP) type II, including a normal urinary cyclic AMP but blunted phosphaturic response to synthetic human parathyroid hormone (PTH), a high level of serum amino-terminal fragment of PTH with a low level of serum calcium and its ionized form, and a high-normal level of nephrogenous cyclic AMP. This patient also had selective hypoaldosteronism, as shown by intermittent hyperkalemia, low plasma and urinary levels of aldosterone and normal glucocorticoid levels. Plasma renin activity was normal but responded to a greater extent to furosemide plus upright posture. Plasma aldosterone was low and responded poorly to furosemide plus upright posture and graded angiotensin II infusions. The possible explanations for the association of PHP type II and selective hypoaldosteronism in this patient with retinitis pigmentosa are discussed.
 ...
PMID:Pseudohypoparathyroidism (PHP) type II and selective hypoaldosteronism in a patient with retinitis pigmentosa. 632 73

Renin secretion from the juxtaglomerular cell is controlled by numerous receptors, humoral agents, and ions. Recently, a stretch receptor hypothesis has been advanced to suggest that all of these diverse factors control renin secretion by a mechanism initiated by a fall in cytoplasmic Ca2+. This fall in Ca2+ may be achieved by lowering Ca2+ influx, raising Ca2+ efflux, or sequestering Ca2+ into cellular organelles and binding sites. The increased renin secretion observed with low arterial pressure, beta-adrenergic agonists, parathyroid hormone, glucagon, cyclic AMP, prostaglandins, low Ca2+ and Ca2+ ionophore, high Mg2+, and Na+ and Cl- may be explained in this context. On the other hand, the decreased renin secretion observed with high pressure, alpha-adrenergic agonists, some prostaglandins, angiotensin, vasopressin, and high K+ may be explained by a rise in cytoplasmic Ca2+ mediated by an opposite sequence of events. Recent observations suggest that the fall in cytoplasmic Ca2+ sets in motion the transport of renin from its site of storage (granules) or synthesis into the cytoplasmic space and finally across the plasma membrane. Thus although renin is stored in granules, its secretion occurs by a process quite different from exocytosis.
 ...
PMID:Cellular mechanisms of renin secretion. 635 57

The pressor effect of arginine vasopressin (AVP) is thought to be mediated by a calcium-dependent mechanism (V1-receptor) whereas its antidiuretic effect depends on c-AMP (V2-receptor). 1-Desamino-8-D-arginine-vasopressin (DDAVP) is possibly an antagonist on the V1-receptor and may therefore be used for assessing the role of endogenous AVP in blood pressure regulation. This possibility was tested using the following models: aggregation of human platelets, renin secretion by rabbit kidney slices, and blood pressure and renin responses in normal human subjects (n = 11) and patients with autonomic insufficiency (n = 4). AVP 10(-10)-10(-7) mol/l caused dose-dependent platelet aggregation and inhibition of renin secretion. These effects were absent in a calcium free medium or in the presence of the calcium antagonist verapamil 5 X 10(-5) mol/l. DDAVP up to 10(-5) mol/l had no effect but shifted the dose-response curves of AVP to the right. AVP infusion into normal subjects is known to lower heart rate and plasma renin with little change in blood pressure. DDAVP 400 ng/kg in 10 min caused no change in systolic pressure but diastolic pressure was lowered by 14 +/- 2 mmHg (mean +/- s.e.m.). Heart rate rose by 24 +/- 2 beats/min and renin rose from 21 +/- 4 to 57 +/- 9 muu/ml (P less than 0.01). In the patients with autonomic insufficiency both systolic and diastolic pressures fell by 20-50 mmHg after DDAVP 200 ng/kg without any change in heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:DDAVP (1-desamino-8-D-arginine vasopressin): an antagonist of the pressor action of endogenous vasopressin? 640 Jan 19


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>