Angiotensin II, effect

In addition to the angiotensin II effects, aldosterone secretion is regulated by increased plasma potassium levels.75,83 Presumably, elevated plasma potassium serves as a stimulus to increase aldosterone release, thus causing increased potassium excretion and a return to normal plasma levels. Finally, there is evidence that ACTH may also play a role in aldosterone release. Although ACTH is primarily involved in controlling glucocorticoid secretion, this hormone may also stimulate mineralocorticoid release to some extent.75... 

Kon V, Flunley TE, Fogo A. Combined antagonism of endothelin A/B receptors links endothelin to vasoconstriction whereas angiotensin II effects fibrosis. Studies in chronic cyclosporine nephrotoxicity in rats.Transplantation 1995 60 89-95. 

Carmines PK, Morrison TK, Navar LG Angiotensin II effects on microvascular diameters of in vitro blood-perfused juxtamed-ullary nephrons. Am J Physiol 251 610-618, 1986... 

The primary effects of angiotensin II ate (/) produciag vasoconstriction directiy or iadirectiy through activation of the adrenergic nervous system ... 

Indapamide has been shown to possess diuretic and iadependent vasodilatory effects (16). It lowers the elevated blood pressure and reduces total peripheral resistance without an iacrease ia heart rate. ladapamide antagoni2es the vasocoastrictiag effects of the catecholamiaes and angiotensin II (16), a property not shared by other thia2ide-type diuretics. Tripamide is also reported to have direct vasodilatory effects (13). 

The kidney contains the major site of renin synthesis, the juxtaglomerular cells in the wall of the afferent arteriole. From these cells, renin is secreted not only into the circulation but also into the renal interstitium. Moreover, the enzyme is produced albeit in low amounts by proximal tubular cells. These cells also synthesize angiotensinogen and ACE. The RAS proteins interact in the renal interstitium and in the proximal tubular lumen to synthesize angiotensin II. In the proximal tubule, angiotensin II activates the sodium/hydrogen exchanger (NHE) that increases sodium reabsorption. Aldosterone elicits the same effect in the distal tubule by activating epithelial sodium channels (ENaC) and the sodium-potassium-ATPase. Thereby, it also induces water reabsotption and potassium secretion. 

The hypotensive effects of most antihypertensive dru are increased when administered with diuretics and other antihypertensives. Many dnigp can interact with the antihypertensive drugs and decrease their effectiveness (eg, antidepressants, monoamine oxidase inhibitors, antihistamines, and sympathomimetic bronchodilators). When the ACE inhibitors are administered with the NSAIDs, their antihypertensive effect may be decreased. Absorption of the ACE inhibitors may be decreased when administered with the antacids. Administration of potassium-sparing diuretics or potassium supplements concurrently with the ACE inhibitors may cause hyperkalemia. When the angiotensin II receptor agonists are administered with... 

Much of the pulmonary NEP activity is believed to reside in the epithelium, as has been demonstrated in the ferret (Borson et al., 1986), and thus it is likely that inhaled ozone would preferentially destroy luminal NEP before affecting any enzymes in the vasculature, which may degrade peptides delivered by the intravenous route. This may explain the route-dependency of BHR after ozone in guinea pigs. Further evidence that the oxidant effects of inhaled ozone are selective is provided by the findings that pressor responses to angiotensin I (which requires conversion by ACE to angiotensin II) were not altered by ozone exposure (Yeadon et eU., 1992). 

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