Production of a Sustained Neurogenic Hypertension of Renal Origin

Abstract

Several methods have been devised for producing experimentally a renal ischemia hypertension. That of Goldblatt, Lynch, Hanzal and Summerville 1 is most frequently used. These methods have all involved the use of a foreign material such as a clamp and have produced blood pressure changes that are not reversible without removing the foreign material or the involved kidney.

It has therefore been difficult to apply these technics to experimental studies analysing the value of various methods of surgical treatment of hypertension in man. It has also been difficult to evaluate the possible importance of a primary nervous factor or a primary vascular disease factor in attempting to correlate experimental renal ischemia hypertension with essential hypertension in man.

A technic has been devised to determine in dogs whether an over-activity of the renal vasoconstrictor splanchnic nerves can produce hypertension. The technic consists of sympathectomizing all of the animal except the origin and the distribution of the splanchnic nerve fibers to the kidneys and adrenals. This is accomplished in 3 operations. At the first the abdominal sympathetic chains below the second lumbar ganglion are removed and the rami to that ganglion as well as the abdominal branches leaving the coeliac ganglion except those to the kidneys are divided. The first lumbar nerve is now cut distal to the origin of the sympathetic ramus. At the second and third operations the first 7 thoracic sympathetic ganglia, including the stellate, are removed and the last 5 intercostal nerves are divided near but distal to the origin of the sympathetic rami on both sides. This leaves the animal completely sympathectomized with the exception of the kidneys and the adrenals.

Five dogs were prepared In the hope that this extensive sympathectomy might produce an overactivity of the remaining portion of the sympathetic system; the innervation of the kidneys and adrenal glands.