Abstract:Background/Aim: Confusing data have been reported about the effect of ethanol or its metabolic products on blood pressure. The pressor agent, angiotensin II (Ang II), is found to be susceptible to degradation by different enzymes known as angiotensinases. We have studied the effects of ethanol and L-NAME, an inhibitor of nitric oxide synthase, consumption on rat serum and kidney ectoenzymes: aminopeptidase N (APN) and aminopeptidase A (APA). Methods: Enzymatic activity of both enzymes was determined spectropho… Show more
“…In a rodent nitric oxide inhibition model of hypertension, i.e., rats treated with N(omega)-nitro-l-arginine methyl ester (L-NAME), less renal, aortic, and serum APN activity than in controls has been reported [84,85]. Although further studies are needed to determine the significance of APN in this model, a decrease in APN activity could be linked to the reported increase in the pressor response to Ang II by decreasing Ang III metabolism [86].…”
Section: Renal Apn In Blood Pressure Regulationmentioning
Aminopeptidase N (APN) or CD13 is a conserved type II integral membrane zinc-dependent metalloprotease in the M1 family of ectoenzymes. APN is abundant in the kidneys and central nervous system. Identified substrates include Angiotensin III (Ang III); neuropeptides, including enkephalins and endorphins; and homones, including kallidan and somatostatin. It is developmentally expressed, a myelomonocytic marker for leukemias, and a receptor for coronovirus. There is evolving support for APN in the regulation of arterial blood pressure and the pathogenesis of hypertension. In rodent strains, intracerebraventricular (i.c.v.) infusions of APN reduces, while inhibitors of APN activity have a pressor effect on blood pressure. Dysregulation of central APN has been linked to the pathogenesis of hypertension in the spontaneously hypertensive rat. There is evidence that renal tubule APN inhibits Na flux and plays a mechanistic role in salt-adaptation. A functional polymorphism of the ANP gene has been identified in the Dahl salt-sensitive rat. Signaling by APN impacting on blood pressure is likely mediated by regulation of the metabolism of Ang III to Ang IV. Whether APN regulates arterial blood pressure in humans or is a therapeutic target for hypertension are subjects for future exploration.
“…In a rodent nitric oxide inhibition model of hypertension, i.e., rats treated with N(omega)-nitro-l-arginine methyl ester (L-NAME), less renal, aortic, and serum APN activity than in controls has been reported [84,85]. Although further studies are needed to determine the significance of APN in this model, a decrease in APN activity could be linked to the reported increase in the pressor response to Ang II by decreasing Ang III metabolism [86].…”
Section: Renal Apn In Blood Pressure Regulationmentioning
Aminopeptidase N (APN) or CD13 is a conserved type II integral membrane zinc-dependent metalloprotease in the M1 family of ectoenzymes. APN is abundant in the kidneys and central nervous system. Identified substrates include Angiotensin III (Ang III); neuropeptides, including enkephalins and endorphins; and homones, including kallidan and somatostatin. It is developmentally expressed, a myelomonocytic marker for leukemias, and a receptor for coronovirus. There is evolving support for APN in the regulation of arterial blood pressure and the pathogenesis of hypertension. In rodent strains, intracerebraventricular (i.c.v.) infusions of APN reduces, while inhibitors of APN activity have a pressor effect on blood pressure. Dysregulation of central APN has been linked to the pathogenesis of hypertension in the spontaneously hypertensive rat. There is evidence that renal tubule APN inhibits Na flux and plays a mechanistic role in salt-adaptation. A functional polymorphism of the ANP gene has been identified in the Dahl salt-sensitive rat. Signaling by APN impacting on blood pressure is likely mediated by regulation of the metabolism of Ang III to Ang IV. Whether APN regulates arterial blood pressure in humans or is a therapeutic target for hypertension are subjects for future exploration.
“…The effects of alcohol on the degree of liver injury depend on the dose, sex and age, as well on the concentration of alcohol and the length of its usage [3][4][5][6] . Alcohol through its toxic product, acetaldehyde, induces liver damage that can occur in the form of alcoholic fatty infiltration and alcoholic hepatitis, the changes which are reversible upon termination of alcohol intake, and alcoholic cirrhosis, which presents irreversible liver damage 2 .…”
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