Renin Release of Antidiuretic Hormone ADH Research Paper

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Introduction

The renin-angiotensin-aldosterone system (RAAS) plays a very important role in the regulation of systemic vascular resistance and blood volume. Its role helps ensure hemodynamic stability when the body loses water, salt, and blood. The baroceptor reflex always corrects these imbalances in a short-term window while the RAAS helps keep the balance when the imbalances are chronic. The RAAS is made up of three main compounds: angiotensin II, aldosterone, and rennin (Weir & Dzau, 1999). The three compounds help in the elevation of blood pressure when renal blood pressure decreases and when there is a decrease in the delivery of salt to the distal convoluted tube. It also increases arterial pressure during beta-agonism. Its characteristics and functions make it possible for the body to regulate blood pressure for long periods of time. While it is mainly linked to the kidneys, its functions also have effects on the adrenal glands, blood vessels, the heart, and the brain.

The Mechanism

Afferent arterioles found in the kidney have specialized cells referred to as juxtaglomerular (JG) cells. The JG cells carry prorenin which is secreted in its inactive form. Its activation in the JG Cells turns it into renin. Its activation is usually triggered by beta-activation or a decrease in blood pressure. The activation may also be due to a response to the reduction of sodium load present in the distal convoluted tubule.

As renin enters the bloodstream, it begins to act on angiotensinogen which is usually produced by the liver and can be found in blood circulation in the plasma. The action of renin on angiotensinogen cleaves it into angiotensin I which is a precursor for angiotensin II. Angiotensin I is naturally inactive (Fountain & Lappin, 2018; Weir, M.R., & Dzau, V.J. (1999).

During the process through which angiotensin I is converted to angiotensin II, an enzyme referred to as angiotensin-converting enzyme (ACE) acts as the catalyst. ACE is mainly found in the lungs’ and the kidneys’ vascular endothelium. On angiotensin I being converted to angiotensin II, it binds itself to angiotensin type I and angiotensin type II thereby affecting the brain, kidneys, arterioles, and the adrenal cortex. It is not yet known conclusively what the type I and type II (AT) receptors roles are. Nonetheless, there is evidence that they have a role in vasodilation through the generation of nitric oxide. While in the plasma, the half-life of angiotensin II is 1 to 2 minutes and then it is degraded by peptidases into angiotensin III and IV (Fountain & Lappin, 2018).

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It has been shown that angiotensin has all the stimulating properties of angiotensin II but only 40 percent of angiotensin II’s pressor effects. The systemic effect of angiotensin IV is reduced.

Angiotensin II increases the reabsorption of sodium in the kidney’s proximal convoluted tubule by increasing Na-H exchange. When sodium levels rise in the body, the blood’s osmolarity increases and this leads to fluid shifting to extracellular space and the blood volume. The increase in blood volume results in high arterial pressure.

The adrenal cortex, particularly the zona gloerulosa, is also acted upon by angiotensin II where it helps in the stimulation of aldosterone release. Aldosterone’s function…

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…with the kidney being one of the places it is dominantly present. It is also highly expressed in the heart and the endothelium. It is the primary metabolism pathway in the heart for AII. When it is deficient, conditions such as progressive cardiac fibrosis and early cardiac hypertrophy may result. These conditions may result in diastolic dysfunction as cardiac pressure overloads or as people age (Macia-Heras et al., 2012). In a failing human heart, ACE2 expression generally increases. This also applies to the levels of A (1 – 7). There has been research done recently on mice showing that increasing the activity of ACE2 may have therapeutic benefits in settings where AII is overactive.

In all, it appears that ACE and ACE2 balance in the heart and the subsequent counterbalancing of AI and A (1-7) are the main factors that drive hypertension and progressive cardiac disease. Data from research done in the area gives support to hypotheses that when the activity or expression of A(1-7) decreases, the cardiovascular system is rendered more vulnerable to AII’s pathological actions (Macia-Heras et al., 2012; Otte & Spier, 2009).

Conclusion

The RAAS has a very important role in the maintenance of water and sodium balance, blood pressure, and vascular tone. It has been shown that its activity is present in renal and cardiac diseases and evaluations are going on to determine if it has a role in the dysfunction in other body organs. Aldosterone and renin ratios are being studied in dogs to help in the identification of primary hypoaldosteronism and primary hypoadrenocorticism. Future studies will be done to….....

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