ABSTRACT
@EN Enhanced activity of renin-angiotensin system (RAS) has been suggested as a cause for the high blood pressure in certain types of experimental hypertension. In spontaneously hypertensive rats (SHR), however, increased RAS has not been found,
the
negative feedback control of renin release by angiotensin Ⅱ and vasopressin has been reported to be altered. Recently, it was suggested that the endogenous adenosine may play an important role in the regulation of renal hemodynamics,
tubuloglomerular
feedback control and renin release. Two subclasses of adenosine receptors, A1 and A2, have been reported to influence renin release from the kidney. However, it has not yet been clarified about the functional subclassification of renal adenosine
receptors. The purpose of these experiments was to determine whether the effect of adenosine analogues on the plasma renin concentration is different is SHR from normotensive Wistar Rats (WR).
N-6-Cyclohexyladenosine (CHA), A1 adenosine agonist, caused dose-dependent decreases in plasma renin concentration (PRC), blood pressure and heart rate in WR. The responsiveness of PRC to CHA in SHR was significantly attenuated but the
responsiveness of
blood pressure was accentuated compared with WR.
5'-N-ethylcarboxamidoadenosine (NECA), A2 adenosine agonist, caused an increase in PRC and decreases in blood pressure and heart rate in WR. The responsiveness of PRC to NECA in SHR was significantly attenuated but that of blood pressure was
accentuated
compared with WR.
2-Chloroadenosine (2 CA) caused decreases in PRC, blood pressure and heart rate in WR. The responsiveness of PRC to 2CA in SHR was attenuated.
These data suggest that the adenosine receptors may be modified in SHR even though the mechanisms involved are unknown. (J Kor Endocrinol 8:42~50, 1993).
|