Abstract
The discovery of atrial, brain, and C-type natriuretic peptides (ANP, BNP, and CNP) and their cognate receptors has greatly increased our knowledge of the control of hypertension and cardiovascular homeostasis. ANP and BNP are potent endogenous hypotensive hormones that elicit natriuretic, diuretic, vasorelaxant, antihypertrophic, antiproliferative, and antiinflammatory effects, largely directed toward the reduction of blood pressure (BP) and cardiovascular diseases (CVDs). The principal receptor involved in the regulatory actions of ANP and BNP is guanylyl cyclase/natriuretic peptide receptor-A (GC-A/NPRA), which produces the intracellular second messenger cGMP. Cellular, biochemical, molecular, genetic, and clinical studies have facilitated understanding of the functional roles of natriuretic peptides (NPs), as well as the functions of their receptors, and signaling mechanisms in CVDs. Transgenic and gene-targeting (gene-knockout and gene-duplication) strategies have produced genetically altered novel mouse models and have advanced our knowledge of the importance of NPs and their receptors at physiological and pathophysiological levels in both normal and disease states. The current review describes the past and recent research on the cellular, molecular, genetic mechanisms and functional roles of the ANP-BNP/NPRA system in the physiology and pathophysiology of cardiovascular homeostasis as well as clinical and diagnostic markers of cardiac disorders and heart failure. However, the therapeutic potentials of NPs and their receptors for the diagnosis and treatment of cardiovascular diseases, including hypertension, heart failure, and stroke have just begun to be expanded. More in-depth investigations are needed in this field to extend the therapeutic use of NPs and their receptors to treat and prevent CVDs.
Highlights
The natriuretic peptides (NPs) family contains a group of hormones that are pivotal in the control of cardiovascular, endocrine, renal, and vascular homeostasis (Brenner et al, 1990; Drewett and Garbers, 1994; de Bold et al, 2001; McGrath et al, 2005; Pandey, 2005a; Rubattu et al, 2006; Kishimoto et al, 2011)
We examined the mechanisms that may mediate the function of increasing numbers of Npr1 gene copies, determining the excretion of urine and sodium, renal blood flow (RBF), glomerular filtration rate (GFR), and blood pressure (BP) after blood volume expansion in Npr1 0-copy, 2-copy, and 4-copy mice in a genedose-dependent manner (Shi et al, 2003)
Our findings demonstrated that the ANP/NP receptor-A (NPRA) axis is predominantly responsible for regulating the renal hemodynamics and Na+ excretory responses to intravascular blood volume expansion. (b) Renovascular Dysfunction ANP-BNP/NPRA system primarily affects glomerulus, tubular, and vascular functions in the kidneys (Nonguchi et al, 1987; Kremer et al, 1988; Light et al, 1989; Appel, 1990; Cermak et al, 1996; Kumar et al, 1997b, 2014; Pandey et al, 2000; Tripathi and Pandey, 2012; Das et al, 2020)
Summary
The natriuretic peptides (NPs) family contains a group of hormones that are pivotal in the control of cardiovascular, endocrine, renal, and vascular homeostasis (Brenner et al, 1990; Drewett and Garbers, 1994; de Bold et al, 2001; McGrath et al, 2005; Pandey, 2005a; Rubattu et al, 2006; Kishimoto et al, 2011).
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