Angiotensin Ii–nitric Oxide Interaction in Glomerular Arterioles

Abstract

1. Resistance changes of the afferent and efferent arterioles determine blood flow and filtration rate in the kidney. The tone of both vessels results from the influence of nerves and humoral and paracrine factors, through a balance of constrictor and dilator systems. Angiotensin (Ang) II and nitric oxide (NO) are important factors determining vascular tone. 2. In the present review, we show that, in addition to the basal production of NO, a specific and significant AngII-induced release of NO occurs in glomerular arterioles. Data from investigations of arteriolar contraction, as well as from fluorescence measurements of NO, in the presence of selective angiotensin AT(1) and AT(2) receptor antagonists indicate an AT(1) receptor-stimulated release of NO in afferent arterioles. 3. The AngII-induced liberation of NO could prevent glomerular arterioles from a marked constriction, particularly in situations of high AngII levels in the kidney.

Angiotensin II Type 2 Receptors and Nitric Oxide Sustain Oxygenation in the Clipped Kidney of Early Goldblatt Hypertensive Rats

“…NO maintains RBF during a high circulating level of Ang II 3,10,11 and thereby maintains blood supply to the kidney during an acute challenge with Ang II. 29 However, the NO released by Ang II from isolated perfused renal afferent arterioles is mediated via AT 1 receptors. 29,30 In contrast, the NO released by Ang II from the kidney cortex of salt-depleted rats or rats with renal wrap hypertension is mediated via AT 2 receptors.…”

“…29 However, the NO released by Ang II from isolated perfused renal afferent arterioles is mediated via AT 1 receptors. 29,30 In contrast, the NO released by Ang II from the kidney cortex of salt-depleted rats or rats with renal wrap hypertension is mediated via AT 2 receptors. [31][32][33] The mRNA for AT 2 receptors is upregulated in the aorta of mice with early 2K,1C hypertension.…”

Angiotensin-(1–7) prevents diabetes-induced cardiovascular dysfunction

“…ANG II overactivity is thought to play a pivotal role in the development of diabetic nephropathy (10,38,46). The glomerular hypertension responsible for diabetic nephropathy results from an interaction between preglomerular capillary vasodilatation provoked by hyperglycemia and postglomerular ANG II-mediated vasoconstriction (18,29,38,46).…”

“…Diabetes-induced cardiovascular dysfunction is evidenced clinically by accelerated atherosclerosis, retinopathy, nephropathy, occlusive vascular disease, and hypertension (18,26,34). Alterations within the renin-angiotensin system are considered to be important for the development of diabetic complications, particularly diabetic renal disease and hypertension (10,38,46,47). Suppression of angiotensin II (ANG II) synthesis or activity can prevent or slow the progression of diabetes-induced cardiovascular complications.…”

Blood Pressure Control in Patients with Glomerulonephritis

“…Vascular endothelium produces vasoactive substances such as nitric oxide (NO) and endothelin (ET). NO preferentially dilates and ET preferentially contract the afferent arterioles (13,14). NO is supposed to participate in the mechanism of increased glomerular filtration in the early stage of diabetic nephropathy, however, the NO synthase inhibition has been shown to increase intraglomerular capillary pressure in experimental glomerulonephritis (15,16).…”