Renin-Angiotensin System and Control of Blood Pressure Essay

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Endocrine control of BP

Hormonal Control of Osmotic pressure: Stimulation

Arterial blood pressure (BP) is under tight control by the mammalian nervous system, cardiovascular system, kidneys, and endocrine system (Vivas et al., 2014). The VII, IX, and X cranial nerves conduct peripheral taste, osmo-sodium, volume, and baroreceptor information to the solitary tract, while the distinct bundles of neurons in the lamina terminalis respond to changes in plasma and cerebral spinal fluid sodium levels, osmolality, and angiotensin II levels. The information thus received is transmitted to the median preoptic, supraoptic, paraventricular, lateral parabrachial, and dorsal raphe nucleus for integration. The neurotransmitter systems involved include angiotensin, vasopressin, oxytocin, and serotonin.

The overall response to reductions in BP and electrolyte content of bodily fluids is to trigger the sympathetic nervous system, endocrine system, and appropriate behavior to correct the deficiency (Vivas et al., 2014). The most important arm of BP control is the renin-angiotensin-aldosterone system, which mediates both short-term and long-term BP regulation (Chopra, Baby, and Jacob, 2011). Plasma angiotensinogen, a 453-aa protein, is produced by the liver and enzymatically cleaved by renin to produce the 10-aa peptide, angiotensin I, which induces mild vasoconstriction. Renin is produced by the juxtaglomerular cells in response to baroreceptor activation due to low BP, detection of low sodium levels in the macula densa ultrafiltrate, and sympathetic nervous system activation (Farrao, Lara, & Lowe, 2014).

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Angiotensin I can be further cleaved by angiotensin converting enzyme-1 (ACE1), primarily in the lungs, to produce the 8-aa angiotensin II, which induces arterial constriction and a measurable increase in BP. ACE1 also inactivates bradykinin, further promoting an increase in BP (Duka et al., 2006).

Angiotensin II mediates its effects through two receptors, AT1 and AT2, each producing opposing activities (Chopra, Baby, and Jacob, 2011). Activation of AT1 induces vasoconstriction, anti-diuresis, anti-natriuresis, cell growth, and proliferation, while activation of AT2 results in vasodilation, dieresis, natruiresis, and anti-proliferation. Although both receptors can be found in tissues throughout the body, the control of BP and the content of body fluids are mediated primarily by receptors expressed in the kidneys (Farrao, Lara, & Lowe, 2014). Angiotensin II will also stimulate anti-diuretic hormone release from the pituitary, thereby promoting increased water reabsorption in the renal collecting ducts, induce aldosterone production from the adrenal cortex, induce sodium reabsorption in the kidneys, and promote potassium and hydrogen excretion through the kidneys. The importance of the kidneys in controlling blood….....

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