Role of ANG II in hypertension produced by chronic inhibition of nitric oxide synthase in conscious rats
M. G. Melaragno and G. D. Fink Department of Pharmacology and Toxicology, Michigan State University, East Lansing 48824-1317, USA. These experiments tested the hypothesis that hypertension caused by chronic inhibition of nitiric oxide synthase (NOS) is associated with augmented pressor responsivenes...
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Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 1996-08, Vol.271 (2), p.H806-H811 |
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Sprache: | eng |
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Zusammenfassung: | M. G. Melaragno and G. D. Fink
Department of Pharmacology and Toxicology, Michigan State University, East Lansing 48824-1317, USA.
These experiments tested the hypothesis that hypertension caused by chronic
inhibition of nitiric oxide synthase (NOS) is associated with augmented
pressor responsiveness to angiotensin II (ANG II). Antagonism of ANG II AT1
receptors with losartan caused a greater fall in blood pressure (BP) in
rats treated for 2 wk with the NOS inhibitor N omega-nitro-L-arginine
methyl ester (L-NAME) than in normotensive rats. The delayed time course of
the decline in BP implicated the slow pressor effect (SPE) of ANG II in
L-NAME hypertension. Further experiments showed that direct elicitation of
the SPE by continuous low-dose (4 ng/min) intravenous infusion of ANG II in
enalapril-treated rats resulted in a larger chronic increase in BP if NOS
was inhibited. However, L-NAME alone also caused a significant increase in
BP in enalapril-treated rats. The combined effect on BP of ANG II and
L-NAME was merely additive. These results confirm that ANG II is involved
in L-NAME hypertension. However, chronic pressor responsiveness to the
peptide is not augmented by L-NAME. |
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ISSN: | 0363-6135 0002-9513 1522-1539 |
DOI: | 10.1152/ajpheart.1996.271.2.H806 |