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EFFECTS OF ATRIAL NATRIURETIC FACTOR ON CYCLIC GMP CONTENT IN THE RAT AORTIC SMOOTH MUSCLE: STUDIES ON THE ROLE OF MEMBRANE Na + ,K + ‐ATPase
Author(s) -
Hegde Sharath S.,
DeFeo Maria L.,
Jandhyala Bhagavan S.
Publication year - 1989
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1989.tb01613.x
Subject(s) - ouabain , medicine , cyclic guanosine monophosphate , endocrinology , guanosine , chemistry , basal (medicine) , antagonism , biology , sodium , biochemistry , nitric oxide , receptor , organic chemistry , insulin
SUMMARY 1. These studies were conducted to determine whether preservation of the functional integrity of the membrane, Na + ,K + ‐stimulated ATPase is essential for the atrial natriuretic factor (r‐ANF‐8–33) to enhance guanosine 3′,5′‐monophosphate (cGMP) content in the rat aortic smooth muscle. In freshly dissected rat aortic tissues, levels of cGMP were estimated using radioimmunoassay. 2. ANF (0.1 μmol/L in Krebs‐Henseleit media) produced significant elevation in cGMP levels in the aortic smooth muscle when compared with that incubated in the control media, whereas suppression of Na + ‐pump with ouabain (1.0 mmol/L) and/or K + ‐free media did not produce any significant changes in the basal cGMP level; these two experimental manoeuvres did not prevent enhancement of cGMP by ANF. 3. Incubation of the tissues in the media containing ouabain plus vasoconstrictor concentrations of norepinephrine (0.3 μmol/L) also did not alter basal cGMP levels and did not prevent the ability of ANF to elevate cGMP. 4. These studies demonstrate that the antagonism by ouabain, of vasorelaxant effects of ANF (as reported in the literature) are not due to the prevention of the ability of ANF to enhance cGMP levels in the arterial smooth muscle. It is proposed that such an antagonism may be related to the actions of ouabain and ANF on diverse, and perhaps independent, mechanisms which affect Ca 2+ ‐fluxes across the cell membrane.