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HyperTension HetuviPareeta Treatment

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Dr. Rajkumar. K.C. MD (Ay) Dr.Srikrishna Khandel MD (Ay),Ph D. Ph. D Scholar Associate Professor,Vikriti Vigyan National Institute of Ayurveda, Jaipur.

The Physiopathology of Hypertension based on ‘Tridosha Sidhanta’ throws light on the treatment principle of this disease in Ayurvedic perspective. Just as cells are structural and functional units, Panchmahabhoota and Tridosha constitute the structural and functional units in Ayurveda. All the solid and hard substances in a cell are “Parthiva”, liquid substances in a cell like fat, water etc. are made up of “Jala”, enzymes, acids, hormones that bring about transformation comprise the “Tejasabhuta”, impulses which are responsible for all movements in and of the cell are formed of “Vayu” and the spaces in the cell that facilitate unobstructed movements are the contributions of “Akasha”. “Parthiva’ and ‘Jala’ effect anabolism. Tejas effects metabolism and ‘ Vayu’ and ‘ Akasha’ bring about energy utilisation, thereby catabolism These three factors scientifically termed as ‘Kapha’ , ‘Pitta’ and ‘Vata’ respectively are the physiological components in Ayurveda. Hypertension , which is over activity of circulatory system enhances catabolic activity and could easily be perceived as an aggravated vata disease. As most of the symptoms like pulsating headache, giddiness (bhrama), palpitation(spandanam), insomnia (nidra nasha), nervousness(anavasthita chittata), fatigue (balabhramsha) etc. identify well with the deranged vata symptoms, hypertension in Ayurveda could be considered as a disease of vitiated vata or a ‘nanatmaja vata vyadhi.’.

Blood pressure (B.P) is the result of cardiac output and peripheral resistance. Cardiac output (systolic blood pressure) depends on salt intake, renal function, mineralocorticoids, heart rate and contractility. Peripheral resistance depends on vasoconstriction mediated by sympathetic alpha receptors, chemical mediators like angiotensin, catecholamines (adrenaline, noradrenaline and dopamine), local hormones etc. ‘Chalatva’ and ‘laghutva’ are the two ‘gunas’, which are needed for the smooth functioning of circulation. These ‘gunas’ act properly in the ‘vatavahasrotas’ when there is a balance between parasympathetic and sympathetic (alpha and beta receptor) functions and also harmonious activities of hormones (endocrine, local substances and chemical mediators) on this ‘srotas’. Chalatva is regulated by various mechanisms viz 1. Dosha Prakriti 2. state of Prana 3. State of Vyana .4. state of Agni 5. srotashudhi (Akasha) 6. mental state. Thus ‘chalatva’ (dysfunctioning of ‘Prana’ and ‘Vyana’) effecting ‘Vatavahasrotas overactivity is the cause of Hypertension.

During systole, part of energy of myocardial contraction is expended in propelling the blood through the arterial tree and part in distending the large arteries. During diastole elastic recoil of the arterial wall maintains the diastolic pressure. Unimpaired muscular activity (bala), energy utilisation (oorja) and propulsion (prayatna) are the functions of udana in circulation. ‘Vishada’ is the property that obstructs energy utilisation (Ajeevana-Sushruta Sutra 46/517-Dalhana) and laghu’ is the property that prevents development of fatigue (Asaadakara) by facilitating smooth functoning. ‘Vishada’ cleanses the channels and ‘laghu’ which is having ‘ Akasha- Vayu- Agni’ constitution facilitates normal hormonal activities and energy utilisation in ‘Vatavaha srotas’ . Thyroxine vitiates udana and increases cardiac output, there by systolic B.P. Exercise practiced according to one’s capability induces ‘laghutva’ and ‘ Karma saamarthya’, while ‘oorjaskara’ medicines bring about normalcy of ‘Udana’ . Bala (force of contraction of heart) is regulated by several mechanisms. 1. Sara prakriti. 2. Samhanana ( Yuktikrita) 3. Udana (Oorja and laghu-Oxygen and nourishment available and utilised) 4. Season 5. Elasticity ( ‘Sthithisthapakatva’ of blood vessels) and 6. Bala vridhikara bhavas (youth, happiness etc.).Thus increase in laghu and Vishada results in Udana dysfunction, Bala Kshaya and thereby hypertrophy and cardiac failure.

Vasomotor centre is situated in the reticular formation of medulla oblongata. Vasomotor tone is the continuous discharge of impulses from vasoconstrictor center through vasoconstrictor nerve fibers (sympathetic adrenergic fibers by secreting noradrenaline). Vasomotor tone maintains arterial blood pressure by producing constant partial constriction of blood vessels. Individuals with persistent essential hypertension will have increased vascular smooth muscle tone. As a result peripheral resistance remains high. This is the state when the patient has established hypertension with the onset of concomitant vascular damage. Thus essential hypertension is the pathological state of Prana which imparts its effect on ‘madhyamaroga marga’, ‘Hridaya’, ‘Budhi’ and ‘Indriya’. Anterior and posterior pituitary hormones regulate B.P by acting on adrenal cortex hormones (Vata vaha srotas)and kidneys (Udakavaha srotas) respectively.

When arterial blood pressure falls kidney secretes renin. Renin acts on angiotensinogen and converts it into Angiotensin I. Angiotensin I is converted to Angiotensin II by Angiotensin Converting Enzyme (ACE). Angiotensin II increases B.P by two ways l.By vasoconstriction (Sankocha) 2. By the release of aldosterone from adrenal cortex .Aldosterone causes retension of water and sodium leading to further increase in B.P by regulating extra cellular fluid ( Kleda). The equilibrium of ‘udaka’ in the body is maintained by several feed back type regulatory mechanisms like sweating, thirst and micturition reflexes, Rasa dhatvagni and Apya bhutagni activities and also by Apana- prana -Vyana cycle. When the function of ‘Apana’ and ‘vegapravritti’ are distrubed, ‘Prana’ who is the controller of urges gets stimulated who in turn stimulates Vyana situated in the heart.

Autoregulation is an intrinsic capability of the arterioles in the vascular beds to regulate the flow of blood. This regulation depends on the quantity of blood available and the metabolic needs of the surrounding tissues along with the concentration of metabolites (dhatu-mala) in the blood. Vascular endothelial cells can release both dilator and constrictor substances. According to the autoregulatory hypothesis primary Hypertension begins with increased cardiac output. Velocity of blood flow, volume and viscosity of blood indirectly (through local hormones) affect the ‘Vatic’ functions. The pathology developing in this disease is neither ‘raktagatavata’ (as vitiated Vata is not located in rakta) nor ‘raktavrita Vata’ (vitiated rakta is not causing obstruction in ‘vata vaha srotas’, and moreover Hypertension is the overactivity of ‘vatavaha srotas’ rather than ‘rakta vaha srotas’). Hypertension may develop in Anaemia (Rasa vaha sroto dushti and Rakta Kshaya) to meet the increased oxygen demand. ‘Jaleeya’ substances in the body are Kapha, Pitta, vasa, rasa, rakta, mutra, sweda etc. ‘Kleda’ denotes metabolic (endogenous) water and other unwanted substances that are to be eliminated through urine or sweat. When the circulatory fluid reaches ‘Vasti’, ‘Kleda’ gets filtered. Occlusion of renal artery or dietary salt restriction leads to increased secretion of renin by the kidney and set up renin – Angiotensin – Aldosterone system. The functions of this system are antagonized by Atrial Natriuretic factor (ANF increases urinary excretion of sodium), a hormone secreted by specialized cells located in cardiac atria. ANF opposes the vasoconstrictor effects of Angiotensin II. The vasculature responds quickly to the hemodynamic changes in the tissue by autoregulation. Salt has maximum ‘ushnatva’ among tastes. Excess salt, fear etc bring about udakavahasrotodushti and hemodynamic changes effecting autoregulation and Hypertension. These changes are brought about by ‘vegaaghaata’ (vasoconstriction and sodium reabsorption) and ‘Udavarta’ (increased sympathetic out flow). Body (Prana) tries to regulate this ‘Udavarta’ resulting in increased vasomotor tone and cardiac output.

Sympathetic nerves, catecholamines and corticosteroids cause adrenergic stimulation via beta receptors. Thyroxine increases systolic pressure by increasing cardiac output. Vasopressin (ADH), Angiotensin and serotonin (5HT) cause vasoconstriction. Local vasoconstrictors act through hormones and chemical mediators. Living tissue is ever changing and dynamic. Cells have to adapt (saatmyam) to this by continuously changing and adopting themselves according to the cues presented by the environment. Thus the body adjusts the nature and path of the 4 impulse through hormones, mediators and receptors. Minerals (Potassium, Calcium, Magnesium) determine the state of ‘Srotas’. Neurotransmission (chalatva), maintenance of osmotic gradients (Aapyabhutagni) and pH balance (equilibrium of kleda- Rakta shudhi) are the important electrolyte functions.Oxygen deprivation (Vaishadya) is accompanied by electrolyte disturbances. Thus ‘Vatavaha srotas’ functioning is carried out and regulated by ‘Agni’, ‘Prakriti’, ‘Saatmya’, nature of vata etc.

Acharya Sushruta states that the functions performed by ‘rasa’ are genetically determined by the deeds of preceding life (Sutra 14/3). So the diameter of vessel wall, (coarctation of aorta), susceptibility to develop Hypertension etc. are predestined.