Effect of prostaglandin E1 on renin in the dog

Werning, C; Vetter, W; Weidmann, P; Hu, Schweikert; Stiel, D; Siegenthaler, W

doi:10.1152/ajplegacy.1971.220.4.852

Cited by 87 publications

(29 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…When active sodium potassium exchange is maximally inhibited with ouabain, a small component of sodium efflux remains which can be inhibited by ethacrynic acid. Whether this represents a second sodium pump, as suggested by Hoffman, or whether it represents exchange diffusion is not completely clear (17,14). Gardner et a/.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Effect of Treatment with Prostaglandin Synthetase Inhibitors on the Erythrocyte Sodium Transport Abnormality of Bartter's Syndrome

Cole

O’Regan

1981

Pediatr Res

View full text Add to dashboard Cite

Section: Resultsmentioning

confidence: 99%

“…Increased plasma levels of PGEz could in turn lead to hyperreninemia, increased plasma aldosterone, and low potassium (8,9,17). The reason for increased PGEz production in Bartter's syndrome has not yet been elucidated (9,16).…”

Section: Resultsmentioning

confidence: 99%

Effect of Treatment with Prostaglandin Synthetase Inhibitors on the Erythrocyte Sodium Transport Abnormality of Bartter's Syndrome

Cole

O’Regan

1981

Pediatr Res

View full text Add to dashboard Cite

“…In detail, there is broad evidence that substances activating the adenylate cyclase on the one hand, like fl-catecholamines [26,39], prostaglandins [34,35,82,83], glucagone [75,78], parathyroid hormone [63,67] and on the other hand dibutyryl-cAMP [2,52] all stimulate renin release. Furthermore, inhibition of cAMP phosphodiesterase also leads to a stimulation of renin release [60,80].…”

Section: Role Of Cyclic Amp For the Intracellular Control Of Renin Rementioning

confidence: 99%

Intracellular control of renin release — An overview

Kurtz

1986

Klin Wochenschr

View full text Add to dashboard Cite

The renin angiotensin aldosterone system is an important regulator of the extracellular volume and of the control of blood pressure. It is mainly controlled in its activity by the rate of renin release from the kidney. Within the kidney renin is produced, stored and released from the so-called granular juxtaglomerular cells. These cells are modified smooth muscle cells and are found in the tunica media of the afferent arteriole, just adjacent to the glomerulus. They resemble morphologically vascular smooth muscle cells but have also characteristic features of secretory cells with respect to a welldeveloped endoplasmic reticulum, a prominent Golgi-apparatus and membrane bound granules containing renin [6,73].Since the rate of renin release from juxtaglomerular cells has a direct effect on blood pressure and because an enhanced rate of renin release is known to be a major reason of hypertension, the mechanisms controlling renal renin release have attracted considerable interest among physiologists, pharmacologists and clinicians.So far four basic mechanisms controlling renin release from the kidney have been described [26]. These comprise 1. The intra-renal blood pressure, which influences renin release by an as yet undefined baroreceptor.2. The amount of NaCl-load sensed by the macula densa segment of the distal tubule (macula densa sensor).3. The sympathetic nervous system 4. A large number of humoral factors like catecholamines, angiotensin II, vasopressin, atrial natriuretic peptide as well as metabolites as for example adenosine.In spite of the large body of findings about the modulation and alteration of renal renin release, the intracellular mechanisms by which renin release is controlled within the juxtaglomerular cells are not clearly understood.During the last years the mechanisms of physiological and pharmacological alterations of renin release have been reviewed [26, 36, 39]. The present contribution wants to concentrate on the intracellular processes that influence renin release from juxtaglomerular cells. The available information will be discussed in front of the background of the present knowledge about the general mechanisms of secretion.For a variety of secretory cells including adrenal medulla and cortex, pituitary, exocrine and endocrine pancreas, neutrophils and platelets it has been found that the secretory process is triggered by the intracellular levels of calcium and cyclic nucleotides and further by the activity of protein kinase C [12,33,64,68,[70][71][72]. I shall therefore discuss in special the role of intracellular calcium, intracellular cyclic AMP and cyclic GMP and protein kinase C activity in the control of renin release from juxtaglomerular cells. In this context I will also present our own results obtained from studies on the intracellular control of renin release from isolated juxtaglomerular cells. Role of Calcium in the Intracellular Control of Renin ReleaseThe typical secretory process in a large number of secreting cells has been found to be biphasic. The secretory process ...

show abstract

“…In animal studies, indomethacin inhibited the renin release in rabbits (Larsson et al, 1974). In the similar ways, a significant increase of PRA was observed by the infusion of PGE1 in dogs (Werning et al, 1971). PGE1 stimulated the release of renin from cell suspensions of rabbit renal cortex (Dew and Michelakis, 1974).…”

Section: Discussionmentioning

confidence: 83%

Effect of prostaglandin E1 on renin and aldosterone in hypertensive patients.

Yoshimura¹,

Takahashi²,

Takashina³

et al. 1979

Endocrinol Japon

View full text Add to dashboard Cite

SynopsisThe effect of prostaglandin E1 (PGE1) on plasma renin activity (PRA) and plasma aldosterone concentration (PAC) was studied in the hypertensive subjects treated with or without75mg indomethacin or60mg propranolol for a week. Subsequent to the treatment with indomethacin for a week, PRA and PAC levels were decreased as compared to the control, without changes in the blood pressure and heart rate. During the infusion of PGE1, the blood pressure was decreased and the pulse rate was increased. PRA and PAC levels were also elevated. These changes of parameters were not different between the control and the indomethacin-treated subjects. PRA and PAC were suppressed after the treatment with propranolol.With the infusion of PGE1, the level of PRA was not significantly elevated, while, PAC was significantly increased by the infusion of100ng/Kg/min of PGE1. During the infusion of PGE1, the blood pressure was decreased while the pulse rate was increased in the subjects treated with propranolol.However, the elevation of the pulse rate was less remarkable than the control. These data indicate that PGE, have important roles in the regulation of the release of renin and aldosterone.These findings also suggest that PGE1 may act to stimulate the secretion of aldosterone in man.Prostaglandins of E series (PGEs) cause vasodilatation and natriuresis and these factors may play important roles in the regulation of blood pressure.The vasodilating effect of PGEs may be mediated by the changes in circulating blood levels of the hormones or by alterations in concentration of PGEs in vascular walls (Anderson et al., 1976).It is believed that PGEs have an important role in the regulation of the renin-angiotensin-aldosterone system. Many investigations have been reported about the effect of exogenous PGEs on renin and aldosterone, and also about the effect of an inhibitor of PGs synthesis on renin and aldosterone (Fichman et al., 1972; FOlich et al., 1976;Golub et al., 1976).These investigations indicate that endogenous PGEs may act to stimulate the release of renin. Similarly many studies examining the effect of PGs on aldosterone secretion have been performed.As aldosterone secretion is regulated by the trophic stimuli of angiotensin II (A II) and ACTH and also by potassium and a decreased serum sodium, it is hard to estimate the single factor that stimulates aldosterone secretion during the administration of PGEs. Fichman et al.,(1972) demonstrated that nonvasodepressor doses of prostaglandin A1 (PGA1) increased plasma aldosterone concentration (PAC) in the absence of a rise in plasma renin activity (PRA) in Received December5, 1978.

show abstract

Effect of prostaglandin E1 on renin in the dog

Cited by 87 publications

References 0 publications

Effect of Treatment with Prostaglandin Synthetase Inhibitors on the Erythrocyte Sodium Transport Abnormality of Bartter's Syndrome

Effect of Treatment with Prostaglandin Synthetase Inhibitors on the Erythrocyte Sodium Transport Abnormality of Bartter's Syndrome

Intracellular control of renin release — An overview

Effect of prostaglandin E1 on renin and aldosterone in hypertensive patients.

Contact Info

Product

Resources

About