Metabolic characteristics of aorta from spontaneously hypertensive and renal and deoxycorticosterone acetate-salt hypertensive rats.

Abstract

SUMMARY The purpose of this study was to determine if any changes occurred in the basal and stimulated rates of oxygen consumption and lactate production of thoracic aortas from spontaneously hypertensive rats (SHR) and renal and deoxycorticosterone acetate (DOCA)-salt hypertensive rats, and, if so, whether these changes were similar in these three models of hypertension. Rings of thoracic aorta were placed in an isothermic (37°C) muscle bath, and isometric tension development, oxygen consumption, and lactate production were measured. The results indicated that under basal conditions oxygen consumption, but not lactate production, was higher in aortas from all three hypertensive models; the elevation above control was greatest in the renal model (95%) and smallest in SHR (34%). On stimulation with 60 mM KCI, a significant increase in oxygen consumption above basal value occurred in all aorta samples (p < 0.05); however, lactate production was increased above basal only in aortas from hypertensive animals. Only in aortas from renal and DOCA-salt models was the rate of oxygen consumption during stimulation significantly greater than that of their normotensive controls (p < 0.05). Developed active stress in response to KCI was the same in all groups, and when the change in lactate production or oxygen consumption was expressed relative to the amount of active stress developed, no differences were observed. These results suggest that, 1) compared to values in aortas from normotensive animals, only the basal rate of oxygen consumption is higher; 2) this higher level of basal metabolic activity is not associated with an alteration in the metabolic cost of force development; and 3) there are quantitative differences between the models with regard to their metabolic characteristics. ( Received July 24, 1984; accepted July 22, 1985. aortas from renal hypertensive rats. These studies suggested that an increase of metabolic activity occurred in association with hypertension; however, a limitation of these studies was that the contractile state of the tissue was not determined when the metabolic parameters were measured and, therefore, the observed elevation in metabolic rate may have been due to a higher level of contractile activity in the tissue from the hypertensive animals. Arner and Hellstrand 3 and McMahon and Paul 4 improved these measurements by using an isolated tissue bath in which force, oxygen consumption, and lactate production were measured simultaneously to study aortas from spontaneously hypertensive rats (SHR) and aldosterone-salt hypertensive rats, respectively.A comparison of these two studies 3 4 indicates that the metabolic changes associated with these two hypertensive models may not be the same.

Immunolocalization of native antioxidant scavenger enzymes in early hypertensive and atherosclerotic arteries. Role of oxygen free radicals.

“…Increased mural oxygen consumption also has been reported by others in experimental hypertension. 14 Furthermore, evidence is mounting that in the hypertensive artery, increased metabolism as well as diffusional limitation may play a significant role in the formation of intimal thickening. 15 Therefore, the heterogeneous mural oxygen distribution in the sequestered subintimal microenvironment may facilitate extensive oxygen free-radical generation.…”

Hypertension induces tissue-specific gene suppression of a fatty acid binding protein in rat aorta.

“…However, relatively little information is available on the nature of the cellular responses to hypertension in the arterial wall and the biochemical mechanisms mediating those responses. In the aorta, hypertension has been shown to induce alterations in connective tissue metabolism (2), lysosomal enzymes (3),'ion transport (4), and fuel metabolism (5,6). A variety of morphologic changes involving cellular components and extracellular matrix also have been described (7)(8)(9).…”

Heightened respiratory‐parasympathetic coupling to airways in the spontaneously hypertensive rat

“…Minute ventilation, blood gases, blood pH and base excess are all comparable between SH and WKY rats breathing normoxia at rest (Wennberg et al 1984;Tian et al 2019). However, there is evidence of a higher metabolic rate in the SH rat versus the WKY, meaning a greater oxygen demand in some tissues (Seidel & Strong, 1986;Dodd et al 2012). This may lower the threshold for tissue hypoxia in SH rats, which may explain a number of compensatory mechanisms, such as the exaggerated chemoreflex evoked respiratory responses to hypoxia in SH rats (Sabino et al 2016;Tian et al 2019;Zera et al 2019).…”