Introductory Remarks Concerning Neural Factors in Essential Hypertension

The vasoconstrictor effect of neural stimuli from frontal and hypothalamiic centers to the blood vessels, including the renal arterioles, is reviewed. Such a theory of the pathogenesis of hy-pertension is probably deficient, since huinoral or atherogenic factors also play a part. Never-theless, splanchnicectomy may sometimes alleviate superimposed vasoconstriction and help ill treatment of the patient. MY INTEREST in hypertension began when I assisted Dr. Max Peet at his first splanchnic section for hypertension in 1933. The patient was an extremely sick 29-year-old man whose blood pressure did not drop below 260/150 mm. Hg on bed rest. He was almost blind from hemorrhages and exu-lates and showed papilledema of 4 diopters. We would now consider the operation on this patient an inadequate sympathectomy al-though the splanchnic nerves were divided. The patient's blood pressure, nevertheless, fell to normal and remained there for almost 10 years, his vision becoming perfect. The theory on the basis of which Dr. Peet performed his first splanchnicectomy was that of shunting the blood from the peripheral cir-culation into the splanchnic area, thus pro-viding a safety valve. He also believed that splanchnic section would diminish neurogenic adrenal secretion. When the work of Dr. Goldblatt appeared we realized that there might be a third mechanism that the operation relieved when it was successful, that is, renal vasoconstriction. I visited Dr. Goldblatt soon after his first paper appeared, and will never forget his kindness and modesty, nor his reti-cetnce in accepting our belief that splanchnic section might relieve essential hypertension by removing the theoretical Goldblatt clamps of renal vasoconstriction