New Histopathologic Evidence for the Parasympathetic Innervation of the Kidney and the Mechanism of Hypertension Following Subarachnoid Hemorrhage

Abstract

Background: the Cushing response was first described in 1901. One of its components is elevated systemic blood pressure secondary to raised intracranial pressure. However, controversy still exists in its pathophysiologic mechanism. Hypertension is attributed to sympathetic overactivity and vagotomy increased renal-based hypertension. However, the role of the parasympathetic system in hypertension has not been investigated. This subject was investigated following subarachnoid hemorrhage (SAH). Methods: A total of 24 rabbits were used: control group (n = 5), SHAM group (n = 5), and an SAH group (n = 14; bolus injection of blood into the cisterna magna). Blood pressures were examined before, during, and after the experiment. After 3 weeks, animals were decapitated under general anesthesia. Vagal nodose ganglion, axonal degeneration, and renal artery vasospasm (RAV) indexes of all animals were determined histopathologically. Results: Significant degenerative changes were detected in the vagal axons and nodose ganglia following SAH in animals with severe hypertension. the mean degenerated neuron density of nodose ganglions, vasospasm index (VSI) values of renal arteries of control, SHAM, and study groups were estimated as 9.0 +/- 2.0 mm(3), 1.87 +/- 0.19; 65.0 +/- 12.0 mm(3), 1.91 +/- 0.34; and 986.0 +/- 112.0 mm(3), 2.32 +/- 0.89, consecutively. Blood pressure was measured as 94.0 +/- 10.0 mmHg in control group, 102.0 +/- 12.0 mmHg in SHAM; 112.0 +/- 14.0 mmHg in middle (n = 9); and >122.0 +/- 10.0 mmHg in severe RAV-developed animals (n = 5). Differences VSI values and blood pressure between groups were statistically significant (P < 0.05). Conclusion: the degeneration of vagal nodose ganglion has an important role in RAV and the development of RAV and hypertension following SAH.