In all individuals the rate of increase in blood pressure (dP/dT) is maximal during the waking period. Moreover, the increases in blood pressure begin approximately 1 h before waking and peak 2 h after waking. Changes in heart rate were also maximal during the first 2 h following awakening rising, but no increase in heart rate preceded waking time. As mentioned previously, despite a consistently elevated mean arterial pressure, this rhythmic pattern was maintained in hypertensive volunteers. buy diabetes drugs
The controlling mechanism for this circadian blood pressure/heart rate variation is primarily neurohumoral. In contrast to a predominantly vagotonic state during sleep, the arousal phenomenon is associated with sympathetic stimulation. Wertheimer and associates studied ten normotensive subjects and reported a 24-hour rhythmic variation of blood pressure/heart rate and systolic time intervals that correlated with endogenous catecholamine secretion. Thus, these periodic hemodynamic changes are the consequence of a precise integration between an endogenous biologic clock in the human brain which determines the autonomic tone of the body and the peripheral effects of a timed catecholamine release, both of which are independent of the astronomical cycle of day and night. This synchronized cardiovascular response may be disrupted by abnormalities involving the neural pacemaker, the efferent pathways, target organs, or by the presence of other modulators of cardiovascular function. Attenuated and/or absent circadian related changes in sinus node function are seen in patients with diabetic autonomic neuropathy, transplanted hearts, severe congestive heart failure, hyperthyroidism, and treatment with certain cardiotropic agents. Moreover, in some of these clinical entities a dissociation between the circadian variations of blood pressure/heart rate is also present.
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