Angiotensin II or epinephrine hemodynamic and metabolic responses in the liver of L-NAME induced hypertension and spontaneous hypertensive rats

Abstract

AIMTo study hepatic vasoconstriction and glucose release induced by angiotensin (Ang)II or Epi in rats with pharmacological hypertension and spontaneously hypertensive rat (SHR).METHODSIsolated liver perfusion was performed following portal vein and vena cava cannulation; AngII or epinephrine (Epi) was injected in bolus and portal pressure monitored; glucose release was measured in perfusate aliquots.RESULTSThe portal hypertensive response (PHR) and the glucose release induced by AngII of L-NAME were similar to normal rats (WIS). On the other hand, the PHR induced by Epi in L-NAME was higher whereas the glucose release was lower compared to WIS. Despite the similar glycogen content, glucose release induced by AngII was lower in SHR compared to Wistar-Kyoto rats although both PHR and glucose release induced by Epi in were similar.CONCLUSIONAngII and Epi responses are altered in different ways in these hypertension models. Our results suggest that inhibition of NO production seems to be involved in the hepatic effects induced by Epi but not by AngII; the diminished glucose release induced by AngII in SHR is not related to glycogen content.

UHPLC-DAD characterization of bioactive secondary metabolites from Ocimum americanum and Pupalia lappacea extracts: Antioxidant activity and antihypertensive effects on L-NAME-induced hypertensive rats

“…It is known that L-NAME administration causes a chronic increase in blood pressure in rats model (Gardiner et al, 1990;Babál et al, 1997). The increase in blood pressure could be explained by inhibition of nitric oxide (NO) synthesis by L-NAME (Kimura et al, 2017). Thus, a sufficient amount of NO is associated with normal vasodilatation and normal blood pressure, whereas inhibition of NO production may lead to hypertension (Nyadjeu et al, 2013;Sung et al, 2013).…”