Morphology of renal afferent arterioles in spontaneously hypertensive rats.

Abstract

We present a new perfusion technique that allows arteries down to the level of capillaries to be fixed while relaxed and under a known intravascular pressure. Through a catheter inserted into the right renal artery of 12-week-old male spontaneously hypertensive rats (n=9) and control Wistar-Kyoto rats (n = ll), the kidney vessels were rinsed with human plasma, relaxed by papaverine, and perfused with a casting resin containing microspheres. The microspheres (12 /im) became trapped in the glomeruli of the kidney and, together with a closing of the venous outflow, they caused the flow through the kidney to stop, so that the intravascular pressure was raised to the level of the input perfusion pressure (100 mm Hg). The resin material was allowed to harden, and the kidney was immersion-fixed and prepared for histomorphometrical investigations. This technique made it possible to measure both the structurally determined lumen diameter and the corresponding media thickness under clearly defined conditions. The lumen diameter of afferent arterioles close to the glomeruli showed a 17% reduction in spontaneously hypertensive rats (15.4±0.6 /un; mean±SEM) compared with Wistar-Kyoto rat arterioles (18J±0J /im, p<0.001). However, this was not due to media hypertrophy, because media cross-sectional area was smaller (p<0.001) in spontaneously hypertensive rats (210±6 /un 1 ) compared with Wistar-Kyoto rats (274±16 fim 1 ). We conclude that the lumen reduction in renal afferent arterioles in spontaneously hypertensive rats is not the result of an encroachment on the lumen by a hypertrophic media. (Hypertension 1992^0:821-827) KEY WORDS • arterioles rats, inbred SHR• casts, microvascular • kidney • renal circulation • perfusion • E ven before reliable blood pressure measurements could be made, hypertension was known to be associated with structural abnormalities in all parts of the cardiovascular system, resulting in an increased relation between media thickness and lumen diameter (media:lumen ratio) in the arteries.

Differential effect of T-type voltage-gated Ca2+ channel disruption on renal plasma flow and glomerular filtration rate in vivo

“…In contrast to the present results with mibefradil, NNC 55-0396 inhibited the contraction induced at all K ϩ concentrations, which could be due to variations between patients or, more likely, that the drug also affects L-type Ca 2ϩ channels, as previously suggested (26). Furthermore, an altered function of kidney vascular segments occurs in several pathological conditions, such as diabetes and hypertension (11,39). The present confirmation of a functional role for T-type Ca 2ϩ channels in the regulation of renal function suggests that T-type Ca 2ϩ channels could play a role under physiological conditions as well as in pathophysiological situations.…”

Renal Structural Properties in Prehypertensive Dahl Salt-Sensitive Rats

“…17,20,[31][32][33] This methodology has already been applied for measurements of the vascular structure in SHR by Göthberg and colleagues, 17,20,31 and their results in the vasodilated perfused kidney model are in good agreement with those obtained by other techniques. [21][22][23] In contrast to histological analysis, this technique is accurate and sensitive enough to detect the alterations of lumen in small resistant vessels, because vascular resistance varies inversely with the fourth power of the radius, according to the Poiseuille's law. It can also determine whether the changes of the lumen are confined to the preglomerular or postglomerular circulation.…”

“…Actually, vascular remodeling, vascular hypertrophy, or both occur mainly in the preglomerular resistance vessels, leading to vascular luminal narrowing in the prehypertensive or early hypertensive stage seen in SHR. [17][18][19][20][21][22][23] Thus, in the spontaneous form of hypertension, such as that seen in SHR, it is assumed that these structural changes would promote an increase in renal vascular resistance, especially in the preglomerular vasculature, and thereby serve to maintain normal glomerular pressure in the face of systemic hypertension. 24 The intrarenal hemodynamics characterized by these structural properties is consistent with the hemodynamics obtained in SHR in vivo.…”

Fructose-induced metabolic syndrome is associated with glomerular hypertension and renal microvascular damage in rats

“…Arteriolar morphology was assessed in outer cortical and juxtamedullary (JM) nephrons by indirect peroxidase immunostaining using a monoclonal rat antihuman antibody specific for cardiac, smooth and striated muscle ␣ actin and smooth muscle ␥ actin (Clone HHF35, DAKO, Carpinteria, CA) (15). Afferent arterioles were identified by their location adjacent to the vascular pole of the glomerular tuft, the presence of an internal elastic lamina, and by having fewer thin flattened endothelial cells than the efferent arteriole (25,33). We excluded from measurement all vessels showing more than one layer of endothelium as suggested by Clapp and Croker (4).…”