Experimental models of hypertension in dogs demonstrate that vascular reactivity patterns differ based on the etiology and phase (acute vs. chronic) of hypertension, driven by extrinsic regulatory mechanisms.
Does not inform hypertension management; leaves open whether extrinsic mechanisms predominate across human hypertension etiologies.
The response of the arterial pressure to a variety of drugs acting on different parts of the vascular tree has been employed to determine the contrasting mechanisms of chronic hypertension experimentally produced in dogs. The results suggest that the pattern of response depends on the state of the extrinsic regulatory mechanisms of the blood vessels rather than on intrinsic change in vascular musculature. Contrasting with chronic renal hypertension, greatly increased vasomotor function causes increased peripheral resistance in chronic neurogenic hypertension. The hypertension seems to us to be due more to this increase in resistance than to increased cardiac output. The pattern of vascular responsiveness in acute hypertension is different from the chronic and emphasizes the importance of distinguishing between the two phases of hypertension.
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Page et al. (1951) studied this question.
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