Cardiovascular reactivity in acute and chronic renal hypertensive dogs.

• Experimental renal hypertension might, in part, be due to heightened sensitivity or "augmented cardiovascular reactivity" which we defined as "the degree with which the heart and peripheral vascular system respond to quantitated stimuli." But its measurement in renal hypertensive animals by a number of investigators has yielded conflicting results for many reasons. A distinction is often made between the stage of initiation of experimental renal hypertension and the stage after it has become established. It has been shown by McCubbin et al. that when arterial pressure rises during the initial stage, the carotid sinus baroreceptor resets so as to perpetuate a higher average level of blood pressure. Further, Reed et al. found differences in response to barbiturates and yohimbine during the initial stage compared with the chronic and suggested that the mechanisms of the hypertension differed, the former being humoral, the latter neural. Subsequently, a number of studies have been made almost exclusively using anesthesia and under a variety of experimental conditions. We have re-examined the problem of whether heightened responsiveness to angiotensin, norepinephrine, tyramine, vasopressin, serotonin and, in the case of chronic renal hypertension, l,l-dimethyl-4-pheny]-piperazinium iodide (DMPP), phenylephrine, 3-hydroxy-phenyl ethanolamine and epinephrine occurs in the two different stages of renal hypertension in dogs with and without the use of pentobarbital. Vasoconstrictor responses of