Interactions of adenosine A1 receptor-mediated renal vasoconstriction with endogenous nitric oxide and ANG II
| Autor: | D. A. Droppleman, R. J. Barrett |
|---|---|
| Rok vydání: | 1993 |
| Předmět: |
Male
Agonist Serotonin medicine.medical_specialty Adenosine Purinergic Antagonists Physiology medicine.drug_class Tetrazoles Blood Pressure Arginine Kidney Nitric Oxide Losartan Renal Circulation Rats Sprague-Dawley Phenylephrine Thromboxane A2 Adenosine A1 receptor Heart Rate Internal medicine medicine Animals Angiotensin II receptor type 1 Dose-Response Relationship Drug Chemistry Adenine Angiotensin II Biphenyl Compounds Imidazoles Receptors Purinergic P1 Rats Arginine Vasopressin NG-Nitroarginine Methyl Ester Endocrinology medicine.anatomical_structure Regional Blood Flow Vasoconstriction Renal blood flow cardiovascular system Vascular Resistance medicine.symptom medicine.drug |
| Zdroj: | American Journal of Physiology-Renal Physiology. 265:F651-F659 |
| ISSN: | 1522-1466 1931-857X |
| DOI: | 10.1152/ajprenal.1993.265.5.f651 |
| Popis: | Renal vasoconstrictor responses to the adenosine A1 agonist N6-cyclopentyladenosine (CPA) were compared in the in situ autoperfused rat kidney to responses evoked by angiotensin II (ANG II), endothelin-1 (ET-1), arginine vasopressin (AVP), carbocyclic thromboxane A2 (CTxA2), phenylephrine (PE), and 5-hydroxytryptamine (5-HT). On the basis of their ED50 values (dose of agonist, in mass units, that produced 50% of maximal response to that agonist), the order of vasoconstrictor potency was ANG II > or = AVP > ET-1 > CPA > 5-HT > or = PE > CTxA2. Dose-response curves to CPA were shallower and maximal responses were weaker than those produced by the other agonists. Maximal responses, the log ED50, and the slope of the dose-response curve to CPA were markedly potentiated in the presence of the nitric oxide (NO) synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME). Selective antagonism of A1 receptors increased renal blood flow and markedly attenuated CPA-induced renal vasoconstriction in the absence or presence of L-NAME but had no effect on the maximal responses to ANG II. Conversely, AT1 receptor antagonism attenuated renal vasoconstriction produced by ANG II but had little effect on the produced by CPA. These results suggest that endogenous NO modulates renal vasoconstriction produced by A1 receptor stimulation and provide evidence against an interaction between renovascular adenosine A1 and angiotensin AT1 receptors. |
| Databáze: | OpenAIRE |
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