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Renal thromboxane A2 synthesis in the Lyon hypertensive rat
Author(s) -
Liu KL,
Aissa A Hadj,
Benzoni D.,
Sassard J.
Publication year - 1992
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.1992.tb00129.x
Subject(s) - endocrinology , medicine , prostanoid , thromboxane , thromboxane a2 , stimulation , natriuresis , kidney , chemistry , angiotensin ii , vasoconstriction , thromboxane b2 , thromboxane a synthase , blood pressure , prostaglandin , receptor , platelet
Summary— The aim of the present study was to assess the mechanisms by which norepinephrine (NE) increased the synthesis of prostanoids and revealed a hyperactivity of the Thromboxane (Tx) A2 synthase in the Lyon genetically hypertensive (LH) rat kidney. To this purpose, the effects of NE (1.2 times 10 −8 to 9.6 times 10 −7 M) on renal function and prostanoid synthesis were assessed in isolated perfused kidneys following β‐adrenoceptor blockade by sotalol (10 −5 M) and compared to those of equipressor concentration of an α2‐adrenoceptor agonist, BHT 933 (3.5 times 10 −4 M) and angiotensin II (AII) (7.7 times 10 −9 M). Kidneys were isolated from eight week‐old male LH rats and from their normotensive (LN) and low blood pressure (LL) controls and perfused in a single pass system. In baseline conditions, sotalol did not modify renal function or urinary prostanoids in any of the three strains. Following NE stimulation, it potentiated the increase in renal vascular resistance of LL and LN controls but not that of LH rats. The pressure‐natriuresis and the urinary prostanoids remained unchanged. BHT 933 elicited a weak stimulation of prostanoid release while AII markedly increased it and revealed, as did NE, the hyperactivity of the TxA2 synthase. It is concluded that the NE‐induced stimulation of prostanoid synthesis does not involve β‐adrenoceptors and is unrelated to the associated hemodynamic changes. These results also demonstrate that the increased renal synthesis of TxA 2 observed in LH rat kidney is not a specific response to α‐adrenoceptor stimulation and is likely to involve activation of the phosphoinositide pathway.