1.Angiotensin I conversion by the microcirculation of the nonhuman primate.
Cornish KG;Gilmore JP Blood Vessels. 1981;18(3):128-33.
Previous studies have shown that angiotensin I (AI) is converted to angiotensin II (AII) by converting enzyme (CE) or by tonin. Since all work on tonin has been done in the rodent, its relevance to the primate is yet to be shown. This study examines the conversion of AI to AII by the cheek pouch microcirculation of the monkey (macaca fascicularis). In 9 of the 11 monkeys studied, the conversion of AI to AII was blocked by converting enzyme inhibitor (CEI). However, in 2 older monkeys, AI conversion was not altered by CEI although the vascular response to AI was attenuated by both the AII antagonist (saralasin) and the antibody to AII (Ab-AII). In these 2 older animals, renin substrate caused vasoconstriction that was not altered by CEI, but was reduced by saralasin and Ab-AII. It is concluded that the tonin-angiotensin system is not active in the young macaque, but may be present in the older animals.
2.Angiotensin II signaling promotes follicle growth and dominance in cattle.
Ferreira R;Gasperin B;Rovani M;Santos J;Barreta M;Bohrer R;Price C;Gonçalves PB Endocrinology. 2011 Dec;152(12):4957-65. doi: 10.1210/en.2011-1146. Epub 2011 Oct 18.
It is generally understood that angiotensin II (AngII) promotes follicle atresia in rats, although recent data suggested that this may not be true in cattle. In this study, we aimed to determine in vivo whether AngII alters follicle development in cattle, using intrafollicular injection of AngII or antagonist into the growing dominant follicle or the second largest subordinate follicle. Injection of saralasin, an AngII antagonist, into the growing dominant follicle inhibited follicular growth, and this inhibitory effect was overcome by systemic FSH supplementation. Injection of AngII into the dominant follicle did not affect follicular growth, whereas injection of AngII into the second largest follicle prevented the expected atresia of this subordinate follicle, and the treated follicle grew at the same rate as the dominant follicle for the next 24 h. Inhibition of AngII action in the dominant follicle decreased estradiol concentrations in follicular fluid and the abundance of mRNA encoding aromatase, 3β-hydroxysteroid dehydrogenase, LH receptor, and cyclinD2 in granulosa cells, with minimal effects on theca cells. The effect of AngII on aromatase mRNA levels was confirmed using an in vitro granulosa cell culture system.
3.Cardiovascular effects of centrally injected melittin in hemorrhaged hypotensive rats: the investigation of peripheral mechanisms.
Yalcin M;Savci V Neuropeptides. 2007 Dec;41(6):465-75. Epub 2007 Sep 25.
We have previously shown that centrally injected melittin, a phospholipase A(2) (PLA(2)) activator, increases blood pressure and decreases heart rate in the normotensive conscious rats. In the current study we aimed to determine the cardiovascular effects of melittin in hemorrhaged hypotensive rats and to investigate the mediation of peripheral adrenergic, vasopressinergic and renin angiotensin system in the pressor effect of centrally administrated melittin in both normotensive and hypotensive conditions. Acute hypotensive hemorrhage was performed by withdrawing a total volume of 2.2ml of blood/100g body weight over a period of 10min. Melittin was injected intracerebroventricularly (i.c.v.) at the doses of 1.5microg, 3.0microg or 6.0microg after the stabilization period of hemorrhage procedure. We also repeated previous experiments by injecting melittin (1.5microg, 3.0microg or 6.0microg; i.c.v.) to the normotensive animals. Melittin caused dose- and time-dependent increases in mean arterial pressure (MAP) in normal and hypotensive conditions and decreases in heart rate (HR) in normotensive conscious animals. In hypotensive rats, melittin injected at the dose of 6.0microg completely restored the decrease in blood pressure.
