Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q8IXL6 (RNS)
1,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of atrial natriuretic factor (ANF) on neural control of renin release and sodium excretion by the kidney were examined in pentobarbital-anesthetized dogs. Electrical stimulation of the renal nerves (RNS, 1 Hz) increased the renal secretion rate of renin (RSR) by 627 +/- 141 ng angiotensin I (ANG I)/min and that of norepinephrine (NESR) by 22.2 +/- 5.9 ng/min. Furthermore, urinary sodium excretion (UNaV) was decreased by 59 +/- 7%, with little change in either renal blood flow (RBF) or glomerular filtration rate (GFR). Intrarenal arterial infusion of ANF (alpha-human atrial natriuretic peptide; 10 ng.kg-1.min-1) increased basal UNaV about twofold but had no effect on basal RBF or GFR. The RNS-induced increase in RSR during ANF infusion (198 +/- 117 ng ANG I/min) was significantly lower than that before the infusion (P less than 0.05), whereas the RNS-induced changes in NESR (27.1 +/- 8.5 ng/min) and UNaV (51 +/- 11%) were unaffected. These results suggest that neural stimulation of renin release, but not of tubular sodium reabsorption, can be suppressed by exogenously administered ANF at a dose that does not affect glomerular filtration or renal neurotransmitter release.
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PMID:Atrial natriuretic factor suppresses neural stimulation of renin release in dogs. 257 Dec 99

We investigated alpha adrenoceptor-mediated renin release in relation to renal prostaglandin production in anesthetized dogs. The effects of intrarenally infused phentolamine (5 micrograms/kg/min) on renin and prostaglandin E2 release induced by renal nerve stimulation (RNS, 2.5-5 Hz) were studied in indomethacin (5 mg/kg i.v.)-treated and untreated dogs. In the control group, RNS reduced renal blood flow and increased both renin and prostaglandin E2 secretion rates. Phentolamine inhibited the blood flow response and attenuated the renin response; it did not affect the prostaglandin E2 response. In the indomethacin-treated group, the renal venous plasma prostaglandin E2 concentration was not changed, the renin secretion rate was increased during RNS. Phentolamine also attenuated the renin response in this prostaglandin-depleted state. These results suggest that alpha adrenoceptors participate in renin release induced by RNS and that some of the alpha adrenoceptor-mediated renin release is independent of renal prostaglandins. Prostaglandin release induced by RNS may be mediated by mechanisms other than alpha adrenoceptors.
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PMID:Evidence for prostaglandin-independent mechanisms in renin release mediated by alpha adrenoceptors during renal nerve stimulation in anesthetized dogs. 632 67

The present study was performed in anesthetized dogs to examine the effects of physiological increments in renal arterial plasma osmolality on basal renin secretion rate and on the response of renin secretion rate to RNS. Three concentrations of hypertonic NaCl were infused into the renal artery (i.r.a.) at 0.38 ml/min for 3 min; i.r.a. Hypertonic NaCl at 0.45M, 0.9M, and 1.8M increased the renal arterial plasma osmolality by 6 +/- 2, 8 +/- 2, and 28 +/- 9 mOsm/kg H2O, respectively. NaCl, 0.45M, did not affect renal function, whereas both 0.9M and 1.8M NaCl increased renal blood flow and urinary sodium excretion; neither 0.45M, 0.9M, nor 1.8M NaCl affected renin secretion rate. RNS was applied at two different frequencies: LFRNS and HFRNS. LFRNS did not affect renal blood flow, whereas HFRNS reduced renal blood flow by 50%. Both LFRNS and HFRNS increased renin secretion rate significantly. An i.r.a. infusion of 0.9M NaCl increased urinary sodium excretion and reduced the renin secretion rate response to LFRNS (-52% +/- 15, p less than 0.02) and HFRNS (-25% +/- 8, p less than 0.01). These findings demonstrate that increases in renal arterial plasma osmolality within the physiological range increase renal blood flow but do not affect renal secretion rate. The renal secretion rate response to RNS is attenuated by increased renal arterial plasma osmolality, an effect consistent with increased sodium chloride delivery to the distal tubular macula densa receptor.
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PMID:Effects of physiological increments in renal arterial plasma osmolality on renin secretion rate. 634