Key result
Converting enzyme inhibition (SQ14225) significantly reduced blood pressure in both methylprednisolone-hypertensive and control rats, with a smaller decrease in the former (P<0.05).
Why the study?
The study was conducted to evaluate the renin-angiotensin system via converting enzyme inhibition and angiotensin II sensitivity in sodium-depleted rats with methylprednisolone-induced hypertension.
Answers are grounded in this paper and cite their sources.
Demonstrates that converting enzyme inhibition reduces blood pressure less in glucocorticoid-hypertensive rats than controls, indicating a smaller renin component during sodium depletion.
The renin-angiotensin system was evaluated by inhibition of converting enzyme (CEI) and by testing sensitivity to angiotensin II (AII) in sodium-depleted rats made hypertensive by methylprednisolone (MP), 20 mg/kg im. During a 2-wk period blood pressure rose 38 +/- 4 mmHg (P less than 0.001) in MP and 3 +/- 4 mmHg in controls. After pentobarbital anesthesia, intra-arterial pressure and dose-response curves to AII were determined, before and after SQ14225 (d-3-mercapto-2-methylpropranoyl-l-proline) (1 mg/kg iv). CEI reduced pressure significantly in both MP and controls, although the decrease was smaller in the former (P less than 0.05). Pressor responses to AII were nearly identical in MP and controls and were enhanced to a similar extent by CEI. Ganglionic blockade with pentolinium tartrate, given after CEI, did reduce the pressure in both groups to equal levels. Responses to AII after pentolinium were similar to those obtained after CEI alone. These results indicate that the renin component of glucocorticoid hypertension during sodium deficiency is smaller than that of the normotensive controls. No evidence of glucocorticoid-induced vascular hypersensitivity to AII was detected in this model of experimental hypertension.
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Elijovich et al. (1980) studied Glucocorticoid hypertension in sodium-depleted rats. Converting enzyme inhibition (SQ14225) vs. Normotensive sodium-depleted control rats was evaluated on Intra-arterial blood pressure reduction and pressor responses to angiotensin II (p=<0.05). Converting enzyme inhibition (SQ14225) significantly reduced blood pressure in both methylprednisolone-hypertensive and control rats, with a smaller decrease in the former (P<0.05).
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