Figure 120

Neural and sympathetic influences. The neural reflexes serve as the principal mechanisms for the rapid regulation of arterial pressure. The neural reflexes also exert a long-term role by influencing sodium excretion. The pathways and effectors of the arterial baroreflex and atrial pressure-volume reflex are depicted. The arrows indicate increased or decreased activity in response to an acute reduction in arterial pressure which is sensed by the baroreceptors in the aortic arch and carotid sinus.

The insert depicts the relationship between the arterial blood pressure and baroreflex primary afferent firing rate. At the normal level of mean arterial pressure of approximately 100 mm Hg, the sensitivity (AI/AP) is set at the maximum level. After chronic resetting of the baroreceptors, the peak sensitivity and threshold of activation are shifted to a higher level of arterial pressure.

The cardiovascular reflexes involve high-pressure arterial receptors in the aortic arch and carotid sinus and low-pressure atrial receptors. In response to decreases in arterial pressure or vascular volume, increased sympathetic stimulation participates in short-term control of arterial pressure. This increased stimulation does so by enhancing cardiac performance and stimulating vascular smooth muscle tone, leading to increased total peripheral resistance and decreased capacitance. The direct effects of the sympathetic nervous system on kidney function lead to decreased sodium excretion caused by decreases in filtered load and increases in tubular reabsorption [26].

The decreases in the glomerular filtration rate (GFR) and filtered sodium load are due to increases in both afferent and efferent arteriolar resistances and to decreases in the filtration coefficient (see Fig. 1-7). Sympathetic activation also enhances proximal sodium reabsorption by stimulating the sodium-hydrogen (Na+-H+) exchanger mechanism (see Fig. 1-16) and by increasing the net chloride reabsorption by the thick ascending limb of the loop of Henle. The indirect effects include stimulation of renin secretion and angiotensin II formation, which, as discussed next, also stimulates tubular reabsorption. AI—change in impulse firing; AP—change in pressure; DN—dorsal motor nucleus; NA—nucleus ambiguous; NTS—nucleus tractus solitarii; RBF—renal blood flow; TPR—total peripheral resistance. (Adapted from Vari and Navar [4].)

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