Renin or angiotensinogenase, is the key enzyme produced in kidneys that modulates body’s renin-angiotensin-aldosterone system (RAAS) that mediates volume volume of extracellular fluids such as blood plasma, lymph and interstitial fluid, as well as arterial vasoconstriction. Thus, RENIN regulates the body’s mean arterial blood pressure.
The enzyme renin is secreted by the kidneys from specialized cells called granular cells of the juxtaglomerular apparatus in response to stimuli such as decrease in arterial blood pressure or decrease in blood volume detected by pressure-sensitive cells known as baroceptors, a decrease in sodium chloride levels in the ultrafiltrate of the nephrons, or sympathetic nervous system activity, acting through the beta1 adrenergic receptors.
The renin enzyme produced in kidneys circulates in the blood stream and breaks down angiotensinogen secreted from the liver into angiotensin I.
Angiotensin I is further converted in the lungs by angiotensin-converting enzyme (ACE) into angiotensin II. Angiotensin II is a very potent constrictor of all blood vessels. It acts on the smooth muscle and, therefore, raises the resistance posed by these arteries to the heart. The heart, trying to overcome this increase in its ‘load’, works more vigorously, causing the blood pressure to rise. This is the essential dynamics involved in rise of blood pressure.
Angiotensin I is further converted in the lungs by angiotensin-converting enzyme (ACE) into angiotensin II. Angiotensin II is a very potent constrictor of all blood vessels. It acts on the smooth muscle and, therefore, raises the resistance posed by these arteries to the heart. The heart, trying to overcome this increase in its ‘load’, works more vigorously, causing the blood pressure to rise. This is the essential dynamics involved in rise of blood pressure.
Angiotensin II also acts on the adrenal glands and releases Aldosterone, which stimulates the epithelial cells in the nephrotic tubules and collecting ducts of the kidneys to increase re-absorption of sodium and water, leading to raised blood volume and raised blood pressure.
Aldosterone also acts on the CNS to increase water intake by stimulating thirst, as well as conserving blood volume, by reducing urinary loss through the secretion of Vasopressin from the posterior pituitary gland, resulting in increased blood pressure.
In normal physiological conditions, once the reduced blood pressure is raised to the adequate level, production of RENIN in kidneys is stopped by a NEGATIVE FEEDBACK mechanism, where angiotensin II act upon the special ‘angiotensin II receptors’ on the cell membranes of juxtaglomerular apparatus of kidneys. By this process, level of RENIN in blood stream is maintained with in limits, thereby preventing hypertension. Same way, production of catecholamines such as adrenalin which also plays a role in inducing production of RENIN and maintaining blood pressure high, is stopped by negative feedback action of adrenalin upon adrenogenic receptors on cells of adrenal cortex.
A pathological state of RENIN-ANGIOTENSIN AXIS happens once the NEGATIVE FEED BACK mechanism controlling the production of RENIN is disturbed by inhibition of angiotensin II receptors and adrenergic receptors involved in FEEDBACK process. Such inhibitions may be caused by binding of some pathogenic molecules of exogenous or endogenous origin, having functional groups similar to angiotensin II or adrenalin, so that they can competitively bind to the receptors. This leads to elevated state of RENIN in the circulation, resulting in ESSENTIAL HYPERTENSION.
Modern allopathic drugs are targeted either to block the conversion of angiotensin I into angiotensin II by inhibiting the angiotensin converting enzymes, or blocking the angiotensin II receptors using potent drug molecules. Since such molecular inhibitions may necessarily lead to molecular errors in different essential biochemical pathways, modern antihypertension drugs are prone to produce harmful side effects.
According to MIT concepts, maintaining the plasma level of RENIN by controlling its production by facilitating unhindered NEGATIVE FEED BACK mechanism is the ideal way of treating hypertension without any harmful side effects. Inhibition of FEEDBACK mechanism should be removed by using MOLECULAR IMPRINTS of angiotensin II, adrenalin, or drug molecules having similar functional groups. Various drug substances such as RAUWOLFIA contains a number of bioactive chemicals like ajmaline, aricine, corynanthine, deserpidine lankanescine rauwolscine, rescinnamine, reserpine, reserpiline, isoreserpine, isoreserpiline, serpentinine, and yohimbine, which can inhibit the angiotensin and adrenogenic receptors. As such, POTENTIZED FORMS of such drugs will contain MOLECULAR IMPRINTS that can act as artificial binding sites for binding to the endogenous and exogenous pathogenic molecules which are the causative factors of HYPERTENSION.
According to MIT approach, potentized or MOLECULAR IMPRINT forms of ANGIOTENSIN II, ADRENALIN, CATECHOLAMINES and various DRUG SUBSTANCES that can produce hypertension in crude form will be ideal drugs for treating hypertension without any side effects.
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