Hypertension renin-angiotensin pathway

Because the renin-angiotensin pathway is central to the maintenance of blood volume, arterial blood pressure, and electrolyte balance, abnormalities in this pathway (e.g., excessive release of renin and overproduction of angiotensin II) can contribute to a variety of cardiovascular disorders. Specifically, overactivity of this pathway can result in hypertension or heart failure via the mechanisms previously described. Abnormally high levels of angiotensin II can contribute to hypertension through both rapid and slow pressor responses. Additionally, high levels of angiotensin II can cause cellular hypertrophy and increase both afterload and wall tension. All of these events can cause or exacerbate heart failure. 

Lead nephropathy has also been complicated by the toxicological interactions of chronic kidney disease with adverse cardiovascular effects such as hypertension. Hypertension, as noted in this chapter, is a risk factor for Pb-associated and non-Pb-associated kidney disease, while mechanisms for inducing hypertension include the participation of kidney biochemistry and physiology via, for example, the renin—angiotensin pathway. 

K.-Laflamme, A., Oster, L., Cardinal, R., and de Champlain, J. 1997. Effects of renin-angiotensin blockade on sympathetic reactivity and p-adrenergic pathway in the spontaneously hypertensive rat. Hypertension 30 278-287. 

The peptides are normally formed from a precursor molecule - angiotensinogen - an a2-globulin in the blood, by the action of a 340 amino acid glycoprotein called renin, which acts as an aspartyl protease enzyme (see renin inhibitors). Renin, and its precursor protein, are both stored in the juxtaglomerular cells of the kidney, and release is controlled by three different pathways within the kidney sensitive to Na -transport, blood vessel stretch and Pi-adrenoceptor activation, respectively. Overall, activation of the renin-angiotensin systems is hypertensive, but serves to increase renal perfusion. 

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