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)

1. The effect of intravenous vasoactive intestinal peptide (VIP, 6 pmol/kg per min) on renal function in six patients with cirrhosis of the liver was examined. 2. VIP caused generalized vasodilation and increased plasma renin activity, but diminished the glomerular filtration rate by about one third. 3. The excretion of water, sodium, potassium and calcium also fell significantly. 4. These results differ from our findings in normal man in whom VIP diminished water and electrolyte secretion largely by increasing tubular reabsorption. 5. It is concluded that the elevated VIP levels present in patients with severe liver disease may affect renal function, but that the presence of liver disease may affect renal responses to VIP.
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PMID:Effects of vasoactive intestinal polypeptide infusions on renal function in patients with liver disease. 327 22

VIP has now been shown to produce an increase in renin release in a number of species, including humans. Our work suggests that VIP is capable of producing this effect by a direct action on the renin-secreting juxtaglomerular cells of the kidney. We have found no evidence to support the possibility that VIP produces this effect as a neurotransmitter in the kidney. In this regard, it should be noted that VIP has been identified as a cotransmitter primarily in cholinergic neurons. The kidney is thought to lack cholinergic innervation, and acetylcholine has no effect on renin secretion. We have explored two conditions where renin secretion is known to increase and found that circulating levels of VIP did not increase along with the increase in PRA. Thus, at least in hemorrhage and dietary sodium restriction, VIP does not appear to affect renin secretion through a humoral mechanism. There could be other untested situations where a humoral effect of VIP might come into play since we have shown that the whole animal is capable of increasing plasma VIP to levels that affect renin release. Studies employing recently developed VIP antagonists have the potential to determine in which physiological or pathological situations VIP contributes to the control of renin secretion. For example, in endotoxic shock, plasma levels of both VIP and PRA are significantly elevated. Could the increase in PRA be partly dependent on an action of circulating VIP?
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PMID:Vasoactive intestinal peptide and renin secretion. 329 98

Microelectrode recordings were performed in renin-containing epithelioid (JG) and vascular smooth muscle (VSM) cells of the afferent arteriole in the isolated hydronephrotic mouse kidney. Both cell types had a membrane potential of about -75 mV and exhibited small, spontaneous depolarizing transients, probably resulting from random transmitter release by sympathetic axon terminals. Substances depressing renin secretion, such as angiotensin II, arginine-vasopressin, and alpha 1-adrenergic agents reversibly depolarized both JG and VSM cells. On a molar basis, the action of angiotensin II was strongest. Stimulators of renin release, e.g. isoproterenol, histamine, and prostaglandin E2 did not influence the membrane potential of both cell types. VIP and NPY, possible co-transmitters of norepinephrine, as well as AP II, were also without effect. It is proposed that suppression of renin secretion from JG cells is mediated by depolarization and Ca2+ influx, whereas stimulation is triggered independently from membrane potential changes, e.g. by adenylate cyclase activation.
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PMID:Epithelioid cells: membrane potential changes induced by substances influencing renin secretion. 351 56

Six healthy males received vasoactive intestinal polypeptide (VIP; 6 pmol kg-1 min-1) by intravenous infusion for 90 min, with 60 min control periods before and after. Plasma VIP levels rose by about 100 pmol l-1 during the infusion. VIP produced changes in heart rate and blood pressure consistent with generalized vasodilatation, but there were no significant changes in effective renal plasma flow or glomerular filtration rate. Both plasma solids and haematocrit rose by about 5%, suggesting that haemoconcentration had occurred during VIP infusion. Urine flow fell to about a third, and the fractional excretion of sodium, potassium, chloride and calcium fell to between half and two-thirds of control values. Fractional excretion of phosphate did not fall significantly. Plasma renin activity rose about 3-fold during VIP infusion.
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PMID:Effects of vasoactive intestinal polypeptide on renal function in man. 636 77

VIP containing nerves are present in the kidney and plasma VIP levels are elevated in cardiac failure and severe liver disease. We studied the effects of intravenous VIP; 6 pmol kg-1 min-1 on 6 normal subjects and 3 patients with liver disease. In normal subjects VIP produced flushing and significant rises in heart rate and pulse pressure but the clearance rates of paraaminohippurate and creatinine did not change significantly. Urine flow fell to about 1/3 and the rate of excretion of electrolytes (except phosphate) fell to about a half of control values. Plasma renin activity rose about 3-fold and there were significant rises in haematocrit and the plasma concentrations of solids, calcium and phosphate. The patients with liver disease responded similarly. Elevated plasma VIP could contribute to salt and water retention in disease states.
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PMID:Renal function during vasoactive intestinal peptide (VIP) infusions in normal man and patients with liver disease. 638 98

The effects of a 7-day intraperitoneal infusion with VIP (0.03 nmol.kg-1.min-1) and its antagonist [4-Cl-D-Phe6,Leu17]-VIP (VIP-A; 3 nmol.kg-1.min-1) were studied in sham and bilaterally adrenalectomized rats bearing ACTH and angiotensin II (ANG-II)-responsive adrenocortical autotransplants. VIP significantly increased plasma aldosterone (ALDO) concentration (PAC) and lowered plasma renin activity (PRA) in both groups of animals, without affecting plasma levels of ACTH and corticosterone. This treatment caused a marked hypertrophy of adrenal zona glomerulosa (ZG) and its parenchymal cells (without inducing any significant change in the zona-fasciculata morphology), as well as of ZG-like cells of autotransplants. Isolated ZG cells and autotransplant quarters obtained from VIP-infused rats evidenced a notable increase in both their basal and maximally ACTH- or ANG-II-stimulated ALDO secretion. The simultaneous infusion of rats with VIP-A completely reversed all these effects of VIP. The infusion with VIP-A alone caused, in sham-operated rats, a net decrease in PAC, coupled with a rise in PRA, and a marked atrophy of ZG and ZG cells; basal and maximally stimulated ALDO secretion of dispersed ZG cells was also significantly lowered. Conversely, VIP-A did not evoke any appreciable effect in autotransplanted rats. These findings suggest that endogenous VIP is specifically involved in the maintenance of the growth and secretory capacity of rat adrenal ZG. Since regenerated adrenocortical autotransplants, which are responsive to VIP but not to VIP-A infusion, are completely deprived of chromaffin cells, the hypothesis is advanced that adrenal medulla may be the source of endogenous VIP regulating ZG function.
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PMID:Evidence that endogenous vasoactive intestinal peptide (VIP) plays a role in the maintenance of the growth and steroidogenic capacity of rat adrenal zona glomerulosa. 794 54

Immune cells synthesize, store and secrete hormones, which are identical with the hormones of the endocrine glands. These are: the POMC hormones (ACTH, endorphin), the thyroid system hormones (TRH, TSH, T3), growth hormone (GH), prolactin, melatonin, histamine, serotonin, catecholamines, GnRH, LHRH, hCG, renin, VIP, ANG II. This means that the immune cells contain all of the hormones, which were searched at all and they also have receptors for these hormones. From this point of view the immune cells are similar to the unicells (Tetrahymena), so it can be supposed that these cells retained the properties characteristic at a low level of phylogeny while other cells during the evolution accumulated to form endocrine glands. In contrast to the glandular endocrine cells, immune cells are polyproducers and polyreceivers. As they are mobile cells, they are able to transport the stored hormone to different places (packed transport) or attracted by local factors, accumulate in the neighborhood of the target, synthesizing and secreting hormones locally. This is taking place, e.g. in the case of endorphin, where the accumulating immune cells calms pain caused by the inflammation. The targeted packed transport is more economical than the hormone-pouring to the blood circulation of glandular endocrines and the targeting also cares the other receptor-bearing cells timely not needed the effect. Mostly the immune-effects of immune-cell derived hormones were studied (except endorphin), however, it is not exactly cleared, while the system could have scarcely studied important roles in other cases. The evolutionary aspects and the known as well, as possible roles of immune-endocrine system and their hormones are listed and discussed.
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PMID:Hormones in the immune system and their possible role. A critical review. 2526 40