The pressor responses to noradrenaline, angiotensin and vasopressin were compared in the same dogs under the same conditions serially before and after the production of renal hypertension to observe the role of vascular reactivity in the production of hypertension and to find out the specificity of the changes of vascular reactivity in chronic renal hypertension.
The depressor responses to ganglionic blocking agents and the effects of extensive sympathectomy were also compared in these conditions.
1. The production of experimental renal hypertension in dogs was more frequent by Page's method than Goldblatt's method or their combination.
The period required for producing hypertension was, however, longer.
2. The depressor response to 30 mg/kg of sodium pentobarbital was more marked in the dogs with chronic renal hypertension than normotensive, acute renal hypertensive or neurogenic hypertensive dogs. It took much longer time to restore the original blood pressure level in chronic hypertensives than other groups, suggesting the participation of neural factors in chronic renal hypertension.
3. In the dogs of chronic renal hypertension, the pressor responses to noradrenaline were found to be augmented, but those to angiotensin and pitressin were not enhanced.
4. The depressor responses to a large dose of ganglionic blocking agents in chronic renal hypertension were not significantly different from those in normotensives, although some showed a remarkable responses.
The augmentation to the pressor agents after the administration of the ganglionic blocking agents in chronic hypertensive dogs was similar to that in normotensive control.
5. The extensive sympathectomy in chronic renal hypertensive dogs produced the similar depressor effects to the normotensive control and the blood pressure level after sympathectomy was still higher in the dogs with chronic hypertension.
Therefore, the continuous increase in the vasomotor tone was not remarkable in chronic renal hypertension. Thus, it is concluded that the increase in the vascular reactivity to the sympathetic neurohumoral substance plays a role in the mechanism of the sustained hypertension.
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