Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endothelin (ET-1), a recently discovered endothelium-derived peptide, has been reported to produce potent vasoconstriction in various isolated vessels of experimental animals. Cicletanine (CIC) is a novel antihypertensive agent. This study concerns the effect of CIC on the vascular actions of ET-1 (0.2 nM/kg) and epinephrine (1 microgram/kg) in normotensive Wistar rats. The hemodynamic effects of ET-1 and epinephrine were also tested in the presence of molsidomine (MOL), a vasodilator that releases nitric oxide. Rats were treated for 15 days with CIC (10 mg/kg/day) or gum arabic p.o. Subsequently, the animals were anesthetized and renal and aortic blood flow (BF) determined by pulsed Doppler flowmetry. ET-1 or epinephrine was injected. After return to the basal level, MOL (5 mg/kg) was injected; 10 min later, the mean arterial pressure (MAP) was decreased and then ET-1 or epinephrine was administered. The vascular resistance was calculated by the MAP/BF ratio and expressed as a percentage. In CIC-treated rats, ET-1 induced a renal vasoconstriction smaller than in control rats (+27.2 +/- 5.95 and +60.4 +/- 11.95%, respectively, p less than 0.01). In the presence of MOL, ET-1 produced a smaller increase in MAP (+9.7 +/- 1.34 and +16.9 +/- 2.49 mm Hg, p less than 0.05). Epinephrine injected after MOL in CIC-treated rats induced a smaller renal vasoconstriction than in control rats (+98.8 +/- 29.83 and 185 +/- 30.33%, p less than 0.05). Thus, CIC partially reduced the hypertensive and renal vasoconstrictor effects of ET-1. A combination of CIC and MOL diminished the renal effects of epinephrine. In conclusion, CIC could be used to attenuate the hypertensive status or renal ischemia disorders where ET-1 seems to be implicated.
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PMID:Cicletanine modulates endothelin-induced renal vasoconstriction in the rat. 172 68

The objective of this study was to determine the dose-response effects of epinephrine, given by systemic intravenous infusion to the halothane-anesthetized newborn piglet, on renal blood flow, mean arterial blood pressure, and renal vascular resistance. Seven newborn piglets were acutely instrumented. A transit-time ultrasound flow probe was placed around the renal artery and a femoral arterial catheter was placed for blood pressure monitoring. Epinephrine was infused in doubling doses from 0.2 to 3.2 micrograms.kg-1.min-1. Mean arterial blood pressure increased from 54 mmHg (1 mmHg = 133.3 Pa) to an average of 96 mmHg at 3.2 micrograms.kg-1.min-1 of epinephrine. Renal blood flow increased from 165 mL.min-1 x 100 g-1 at baseline to 185 mL.min-1 x 100 g-1 at a dose of 0.2 microgram.kg-1.min-1 and increased further at 0.4 and 0.8 micrograms.kg-1.min-1 to reach 261 mL.min-1 x 100 g-1. Renal blood flow began to fall at a dose of 3.2 micrograms.kg-1.min-1, remaining however, significantly above baseline (211 mL.min-1 x 100 g-1). Consequently, calculated renal vascular resistance fell as the dose was increased from 0.2 to 0.8 micrograms.kg-1.min-1 and then rose again at 1.6 and 3.2 micrograms.kg-1.min-1, being significantly above baseline at 3.2 micrograms.kg-1.min-1. These results demonstrate that epinephrine when given by systemic infusion to the halothane-anesthetized newborn pig is a renal vasodilator at low doses and causes renal vasoconstriction at moderate to high doses. Renal blood flow remained above baseline at all doses tested, and thus, within the dosage range tested, epinephrine infusion should not cause renal ischemia.
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PMID:Renal vascular effects of epinephrine infusion in the halothane-anesthetized piglet. 792 71