Noradrenergic mechanisms in the brain and peripheral organs of normotensive and spontaneously hypertensive rats at various ages.

Abstract

SUMMARY Previous studies of noradrenergic mechanisms in spontaneously hypertenshe rats (SHR) have yielded conflicting results, as many have used: 1) rats of only one age; 2) a single organ such as heart or brain; or 3) either Wistar-Kyoto (WKY) or an outbred normotensive control rat We have studied the turnover of norepinephrine (NE) in three brain areas (cortex, hypothalamus, brain stem) and three peripheral organs (duodenum, skeletal muscle, kidney) of SHR, WKY, and Wistar rats at 5,9, and 18 weeks of age. The rate of decline of norepinephrine [NE] Presented in part at the Joint Meeting of the American and Canadian Physiological Societies, Toronto, Ontario, October, 1980. Supported by the Ontario Heart Foundation. Address for reprints: Robert L. Kline, Ph.D., Department of Physiology, University of Western Ontario, London, Ontario, Canada N6A 5C1.Received December 12, 1980; revision accepted April 13, 1981. peripheral organs and brain. Many studies have considered the heart as a representative organ of the cardiovascular system, and few have looked at changes in the brain and peripheral organs simultaneously at different ages. Table 1 summarizes the studies of norepinephrine (NE) turnover in SHR that have been published to date.In the present study, we have examined the turnover of NE, a dynamic measure of neuronal function, 1 to determine whether differences in noradrenergic mechanisms exist between SHR and two different normotensive controls, Wistar-Kyoto (WKY) and outbred Wistar rats. Furthermore, as several lines of evidence suggest that neurogenic mechanisms may be involved during the early stages of the hypertensive process in SHR, 2 rats of each strain were studied at 5, 9, and 18 weeks of age. These ages were chosen to represent the pre-or early hypertensive, the rapiddevelopment phase, and the steady maintained phase

Sympathetic Regulation of the Renal Functions in Rats Reciprocally Congenic for Chromosome 1 Blood Pressure Quantitative Trait Locus

“…the estimates for SHRSP and WKY were in good agreement with those reported previously (16,21). These results suggested that RSNA was different among the four strains (25).…”

“…However, due to the technical difficulties posed by the small body sizes of very young rats, we used rats of 6 to 8 weeks of age. At this age, SHRSP rapidly develop hypertension (15,16). Accordingly, a significant difference in BP was observed between the SHRSP-based and the WKY-based strains, while BP was not different between the two SHRSP-based strains nor between the two WKYbased strains.…”

“…At this age, hypertension is not yet established in SHRSP (15,16). Anesthesia was induced by intraperitoneal injection of thiopental sodium (110 mg/kg body weight; Ravonal, Tanabe, Osaka, Japan), which was supplemented via the rectum when needed during the experiment.…”

High-fat diet induces emergence of brown-like adipocytes in white adipose tissue of spontaneously hypertensive rats

“…19 Previous research suggests that (i) brown fat emergence in WAT can be induced by sympathetic b-adrenergic stimulation [20][21][22] and (ii) dietary fat can increase sympathetic outflow from the central nervous system to the periphery. 23 Given these observations, we hypothesized that the spontaneously hypertensive rat (SHR) may be a genetic strain that is susceptible to the emergence of brown fat in WAT in response to a high-fat diet (HFD), as it is characterized by high sympathetic outflow to the periphery, including to WAT, [24][25][26][27] and shows augmentations in sympathetic activity (indicated indirectly by an augmentation in heart rate) 28 and expression of genes involved in fat burning in WAT in response to a chronic HFD. 29 SHR compared with Wistar Kyoto rats, for example, also gain less body weight in response to a chronic HFD.…”

Altered L-DOPA Systems for Blood Pressure Regulation in the Lower Brainstem of Spontaneously Hypertensive Rats.

“…These findings indicate that impaired neuronal L-DOPA release in the NTS of SHR is not secondarily caused by a decrease in the formation or an increase in the decarboxylation of L-DOPA, but apparently arises from the attenuation of arterial baroreceptor reflex processes involved in the release of L-DOPA. Alterations of the catecholaminergic systems in the brainstem have been reported to be involved in the development and maintenance of the hypertension (72)(73)(74)(75)(76). However, our proposed L-DOPA system in the rat NTS differs completely from catecholaminergic systems, as described in the section on normotensive Wistar rats.…”