ANF and angiotensin II interact via kinases in the proximal straight tubule
Autor: | Nestor H. Garcia, Jeffrey L. Garvin |
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Rok vydání: | 1995 |
Předmět: |
Male
medicine.medical_specialty Indoles Physiology Carbazoles Stimulation Absorption Kidney Tubules Proximal Rats Sprague-Dawley Alkaloids Atrial natriuretic peptide 1-Methyl-3-isobutylxanthine Internal medicine Renin–angiotensin system Cyclic AMP otorhinolaryngologic diseases medicine Animals Drug Interactions Protein kinase A Protein kinase C Chemistry Reabsorption Angiotensin II Phosphotransferases Staurosporine Rats Endocrinology Second messenger system cardiovascular system Atrial Natriuretic Factor hormones hormone substitutes and hormone antagonists |
Zdroj: | American Journal of Physiology-Renal Physiology. 268:F730-F735 |
ISSN: | 1522-1466 1931-857X |
Popis: | Atrial natriuretic factor (ANF) inhibits fluid absorption (Jv) in the proximal straight tubule (PST) only after stimulation with angiotensin II (ANG II). To investigate ANF's dependency on ANG II for transport inhibition, we blocked and mimicked angiotensin's second messenger cascades and then examined ANF's ability to inhibit Jv. ANG II (10(-10) M)-stimulated Jv was 0.47 +/- 0.10 nl.mm-1. min-1. After ANF (10(-10) M) was added to the bath, Jv fell by approximately 40% (P < 0.05). ANG II stimulates Jv via activation of protein kinase C (PKC) and decreasing protein kinase A (PKA) activity. We inhibited PKA with H-89. In the presence of only H-89, Jv was 0.75 +/- 0.11 nl.mm-1.min-1. After ANF was added to the bath Jv fell by 30% (P < 0.05). Intracellular adenosine 3',5'-cyclic monophosphate content was not affected by ANF in the presence of ANG II. ANF could not inhibit Jv in the presence of ANG II and 3-isobutyl-1-methylxanthine, a phosphodiesterase inhibitor. KT-5823, a guanosine 3',5'-cyclic monophosphate (cGMP)-dependent protein kinase inhibitor, blocked the action of ANF on Jv (P > 0.30). PKC inhibition did not prevent the decrease in Jv induced by ANF. We conclude that ANF inhibits ANG II-induced stimulation of transport by a mechanism that requires phosphorylation mediated by cGMP-dependent protein kinase subsequent to a decrease of PKA activity. |
Databáze: | OpenAIRE |
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