Hypertension is a dangerous multi-factorial condition that is a dominant factor in diabetes, atherosclerosis, stroke, and kidney disease. It is worsened by vascular stiffness and dysregulated activity of the endocrine and sympathetic nervous systems.
The Renin-Angiotensin System (RAS) is triggered by the cleavage of Angiotensinogen into multiple Angiotensin peptides by Renin, ACE/CD143, ACE-2, and other proteases. Angiotensin peptides regulate hemodynamics through wide ranging actions in the kidney, heart, vasculature, and sympathetic nervous system.
The Endothelin-1 peptide is formed from Big Endothelin by the converting enzymes ECE-1 and ECE-2. It is an extremely potent vasoconstrictor, and it increases cardiac output and cardiomyocyte proliferation. ET-1 signals through type A and type B Endothelin receptors.
In addition to Angiotensin and Endothelin, many vasoactive peptide hormones (e.g. natriuretic peptides, Bradykinin, Vasopressin) contribute to the central and peripheral regulation of blood pressure, vascular tone, and ion homeostasis.
Vascular reactivity is regulated by many classes of small molecules including eicosanoids (e.g. prostaglandins, leukotrienes, thromboxanes), purines, 5-HT/serotonin, histamine, and nitric oxide, plus adrenergic and cholinergic ligands. These molecules induce rapid vasoconstriction or relaxation of the vascular smooth muscle.
Kidney Cell markers
This interactive tool dissects the cell types that make up the renal corpuscle including Bowman’s capsule and the glomerular tuft. It organizes secreted, cell surface, and intracellular molecules for the glomerular and parietal endothelium, macula densa, mesangium, tubule epithelium, podocytes, and also the glomerular basement membrane. Find the reagents and assays you need for research into filtration barrier function, tubule-glomerular feedback, ion homeostasis, and blood pressure control.
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