Lead-induced hypertension: role of oxidative stress.
Orange, United States. In Curr Hypertens Rep, 2004
The pathogenesis of lead-induced hypertension is multifactorial, including such diverse mechanisms as: inactivation of endogenous nitric oxide and downregulation of soluble guanylate cyclase by reactive oxygen species (ROS), leading to a functional deficiency in nitric oxide; heightened sympathetic activity and plasma norepinephrine together with depressed vascular and elevated renal beta-adrenergic receptor density; elevated plasma angiotensin-converting enzyme (ACE) activity, plasma renin activity (PRA), angiotensin II (Ang-II), and aldosterone levels; increased kininase I and kininase II activities; lead-induced inhibition of vascular smooth muscle Na(+)-K+ ATPase, leading to a rise in cellular Na+ and, hence, Ca2+; and a possible rise in endothelin and thromboxane generation.
Role of aminopeptidases in the blood pressure regulation.
Nagoya, Japan. In Biol Pharm Bull, 2004
This review describes the roles of aminopeptidase A, placental leucine aminopeptidase and kininase I, which are enzymes responsible for hydrolyzing angiotensin II (AngII), vasopressin (AVP) and bradykinin (BK), respectively, in BP regulation.
Umbilical plasma kininase I activity in fetal hypoxia.
Nagoya, Japan. In Horm Metab Res, 2003
To shed light on the role of bradykinin in preeclampsia in addition to acute hypoxia, we measured the activity of kininase I, the enzyme responsible for its degradation, in umbilical plasma.
Pathogenesis of lead-induced hypertension: role of oxidative stress.
Irvine, United States. In J Hypertens Suppl, 2002
Several mechanisms have been shown to contribute to the pathogenesis of lead-induced hypertension: (1) avid oxidation and inactivation of endogenous nitric oxide (NO) by reactive oxygen species leading to functional NO deficiency; (2) increased sympathetic activity and circulating noradrenaline coupled with decreased vascular and elevated renal beta-adrenergic receptor density; (3) increased angiotensin-converting enzyme (ACE) activity and elevated plasma renin, angiotensin II and aldosterone levels; (4) heightened kininase I and kininase II activities; (5) possible increase in endothelin and thromboxane production; and (6) lead-mediated inhibition of vascular smooth muscle Na(+)-K+ ATPase leading to a rise in cellular Na+ and hence Ca2+ stores.