Abstract
The spontaneously hypertensive rat (SHR) is a genetic model of primary hypertension with an etiology that includes sympathetic overdrive. To elucidate the neurogenic mechanisms underlying the pathophysiology of this model, we analyzed the dynamic baroreflex response to spontaneous fluctuations in arterial pressure in conscious SHRs, as well as in the Wistar-Kyoto (WKY), the Dahl salt-sensitive, the Dahl salt-resistant, and the Sprague-Dawley rat. Observations revealed the existence of long intermittent periods (lasting up to several minutes) of engagement and disengagement of baroreflex control of heart rate. Analysis of these intermittent periods revealed a predictive relationship between increased mean arterial pressure and progressive baroreflex disengagement that was present in the SHR and WKY strains but absent in others. This relationship yielded the hypothesis that a lower proportion of engagement versus disengagement of the baroreflex in SHR compared with WKY contributes to the hypertension (or increased blood pressure) in SHR compared with WKY. Results of experiments using sinoaortic baroreceptor denervation were consistent with the hypothesis that dysfunction of the baroreflex contributes to the etiology of hypertension in the SHR. Thus, this study provides experimental evidence for the roles of the baroreflex in long-term arterial pressure regulation and in the etiology of primary hypertension in this animal model.
Highlights
Physiological control of arterial blood pressure (BP) is achieved via the interaction of multiple organs and organ systems
The current studies reveal that (a) during normal dark cycle recording the fraction of time the baroreflex control of heart rate (HR) spent in the on state ranged from 40% to 85% for all rat strains observed; (b) the on fraction decreased with age only in the spontaneously hypertensive rat (SHR) and WKY strains; (c) the mean arterial pressure (MAP) was tightly correlated with on fraction in only the SHR and WKY strains; (d) mean pressures during off state were higher than during on state in the SHR and WKY strains for both sexes and at all ages studied; and (e) increases in pressure in the first few days following sinoaortic denervation (SAD) were higher in WKY compared with the SHR
These observations are consistent with the potentially novel hypothesis that the differences in intermittent functioning of the baroreflex play a causal role in the development of hypertension in the SHR strain and the established but still controversial hypothesis that differences in baroreflex function between the WKY and the SHR are partially responsible for the differences in arterial pressure between these strains
Summary
Physiological control of arterial blood pressure (BP) is achieved via the interaction of multiple organs and organ systems. The pressure waveforms in the systemic arteries are governed by the interactions between ventricular pumping and arterial mechanics, the ionotropic and chronotropic state of the heart, and the preloads driving filling of the left and right sides of the heart [1,2,3,4]. These governing processes are in turn regulated by the autonomic nervous system and endocrine signals, notably the baroreflex and the renin-angiotensin-aldosterone system [5,6,7,8]. Because chronic increases in pressure can, in principle, both cause and be caused by mechanical remodeling and changes to autonomic and renal function [7, 10,11,12,13], it is possible that many different primary insults affecting different systems could all drive the system toward the same multifactorial pathological phenotype [14, 15]
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