A critical analysis of role of Raktavaha sroto mula inRaktadushti - Essential hypertension

INTRODUCTION

Hypertension is called a silent killer, because it rarely causes symptoms before it damages the heart, kidney and brain.Hypertension is defined as systolic blood pressure of 140mm of Hg or greater and diastolic BP of 90mm of Hg or greater. When the blood pressure is elevated without an evident organic cause, it is called as essential hypertension.¹

Several etiological factors of Shonita-dusti are also the etiological factors mentioned for hypertension. A category of symptoms of Shonita Dusti pertaining to the psychological change and altered state of consciousness are also similar to the symptoms of Malignant Hypertension. Based on the criteria of naming of disease by their leading symptoms the Shonita Mada is related the symptomatic phase of malignant hypertension. Asymptomatic hypertension can very well be considered as Avyakta stage of the illness or may be simply referred as ShonitaDusti.

Though hypertension is understood based on Nidana and Lakshana of Shonitadusti, the processes or mechanisms operating within, during the asymptomatic stage of hypertension are necessary toanswer. Aggravated, Dosha may cause manifold diseases depending upon the etiological factors and sites of manifestation.² Similarly the affliction of RaktaDusti by Doshas may cause multitudinous illness pertaining to different Srotas.

In the context of Mada, Murcha, Sanyasa Samprapti, it is been explained that based on the strength of etiological factors the disease will gain strength and exhibits the symptoms. The pathophysiological processes associated with ShonitaDusti can be mapped in the same Samprapti. Owing to the etiological factors which vitiate Raktavaha Strotas may also affect Sanjnavaha Srotas. A patient suffering from Sanyasathe Dushti of Rasavaha Srotas alone and or Dushti of Raktavaha Srotas along with Sanjnavaha Srotas is seen. Sanjnavaha or the consciousness is basically governed by Manovaha Dhamani or Srotas.³ Manovaha SrotoSthana is Hridaya.⁴ So Mula of these Srotas are Hridaya, DashaDhamani, Yakrut and Pleeha are sites of Disease manifestation.

The mechanism of Hypertension is not clearly understood but includes four cardinal events. They are increased contractility of myocardium, increased cardiac output, increased peripheral resistance and hypervolemia. These four mechanisms either alone, or together lead to hypertension and which revolve around circulatory system.

1. Increased contractility cf Myocardium - At the level of Hridaya

Cardiac hypertrophy may be an initiating mechanism of hypertension, as a reflection of a primary response to repeated neural stimulation. In young hyperkinetic borderline hypertensive has been explained by neurogenic mechanisms that could be both an increased sympathetic and a decreased parasympathetic drive. Cardiac hypertrophy may also develop as a compensatory mechanism secondary to vascular resistance.

Hridaya is the Moola of Rasavaha Srotus and where VyanaVata is located. Vyanavata is responsible for the circulation of Rasa, Rakta, Ojus and all the Dravadhatu constantly throughout the body through DashaDhamani.⁵ Though Pitta and Raktaare Ashraya Ashrayee, all the Dosha will have an effect on Rakta resulting in different Rakta PradoshajaVikara. For example, Moha, Mada, kampa, Swarakshaya, Gulma etc. are because of Vatakopa, Pittakopa, Kaphakopa. Vyana VataKopa by Rakta Pradoshaja Nidana will have impact over the Hridaya.

ShonitaDusti Nidana can provoke the Dosha which afflicts the ChetasaSthana i.e. Hridaya.⁶ VataDosha is responsible for shaping and gross creation in Parkritaavastha,⁷ may deform the structure of Hridaya in vitiated state. Other conditions like ShonitaDusti, showing involvement of heart as an organ, as seen in hypertension also need to be considered. Thus increased cardiac contractility is attributable to Vitiated Vyana in the Hridaya due to ShonitaDusti.

2. Increased Cardiac Output

Early onset of hypertension is difficult to determine in humans, however, an increased cardiac output without changes in peripheral resistance has been found in some early, borderline hypertensive. Various animal studies have also shown that the initiating hemodynamic disturbance in early hypertension is an increased flow and cardiac output. The increase in cardiac output could logically arise in two ways, either contractility from cardiac hypertrophy or neuronal stimulation.

As per Hareeta, in the context of Pandu, by Nidana, Rakta is vitiated along with Rasa, by the Doshas. Madhukosha. Bringing about paleness to the skin, mechanism explained as vitiated Vyanavata expels the vitiated Rasa out of the heart forcefully.⁸ This expelled pitta vitiated Rasa, is carried to the whole body through the 10 major vessels.Thus finds seat in the Twacha (skin) & produces patches of whitish/pale discoloration, & the disease is named as Pandu.

Vitiated RaktadiDhatu and their forceful expulsion by vitiated Vyanavata from Hridaya through blood vessels is the fact occurring in similar manner in increased cardiac output state of early onset of hypertension.

3.Increased Circulating Fluid Volume

Excess sodium intake and sodium sensitivity can cause hypertension by increasing fluid volume and preload, thereby increasing cardiac output, as well as by effects on vascular reactivity and contractility. The experimental evidence for a role of sodium excess includes: when hypertensives are sodium restricted, their BP falls, even with less rigid restrictions. Exceedingly Lavana, Kshara, Amla and KatuAhara are the prime vitiating factors for Shonita Dusti.⁹ Properties of Lavana explained as Upakledi, visramsanasamartha (to increase fluid volume) and it is said be causing the Shithilatha of Shonita.¹⁰ LavanaRasa also vitiates Pitta Dosha.

There is also direct reference in Charaka sutra Sthanalavana does Raktamvardayathi i.e. volume of the blood will be increased and also causes Kledana, Lohithapitha which indicates that Lavana plays a major role in increase of blood volume.¹¹

Shonitavriddhi explained as Shonitaruptaya Parinantya Rasena Militena.¹² Such phenomena we may observe in Rakta pitta. In the context of Rakta pitta, Ushnaguna of Pitta causing ‘sweating’ of all the tissues i.e. oozing out of liquids from other Dhatus and mixing of all these oozed out fluids like Rasa, Lasika, Sweda into the Rakta, thereby increasing its quantity. This reaches the Yakrut and Pleeha. Thus the hypervolemia of Essential hypertension and its increased pressure on the vessel walls is explained by Pitta and ShonitaDusti Nidana resulting in ShonitaVriddhi at the Srotomula Yakrut and Pleeha.

4.Increased Peripheral Resistance

The final common feature of established hypertension is a raised peripheral resistance, which can be associated with both functional constriction and structural vascular remodeling and hypertrophy. In established hypertension and in the majority of hypertensive patients, no increased cardiac output or no marked excess of any of the known pressure hormones is identifiable.

Ranjakaagni is the name given to pitta situated in the Yakrut, Pleeha, and Amashaya does the ‘Rasa Ranjana’.¹³ one of meaning of Ranjana is colouring and dyeing, which is the leading factor for formation of Rakta from Rasa Dhatu. This can be understood in terms of Iron, B12 or intrinsic factor essential for formation and maturation of RBC.

The another meaning of Ranjana is exhilarating or to stimulate. Many carrier protein molecules are produced from liver which aids in circulation and nourishment. Nitrous oxide, functions as an important signaling molecule in the cardiovascular, nervous. Nitrous oxide is produced from amino acid L arginine. This is carried to various sites bound to the protein which are produced from the liver. From endothelium, it diffuses to smooth muscles cells cause them to relax. Decreases blood pressure and increases blood flow through vessels. In nervous system it acts as a neuro transmitter. But NO is highly unstable and in the presence of antioxidants like vitamin E it is stabilized. Vitamin E also stored in the liver. Reduced production of nitrous oxide and antioxidants lead to an increase in peripheral resistance and manifestation of hypertension.

In the context of Shotha, Vitiation of Vata and it’s seeding in BaahyaSira, leads to their dryness, altered permeability, resulting in increased peripheral resistance. As in Shotha, Dushta VataKaphadi Dosha affects the Sira, because hardening of vessels by afflicting the Rasa Rakta, causing Ruddhagati (Peripheral resistance).

Conclusion

ShonitaMada is related the symptomatic phase of malignant hypertension. Asymptomatic hypertension can very well be considered as Avyakta stage of the illness or may be simply referred as ShonitaDusti. Mula of the Rasavaha, Raktavaha and SanjnavahaSrotas are Hridaya, Dasha Dhamani, Yakrut and Pleeha are the principle seat of the pathology. In a complex pathological process of ShonitaDusti, Yakrut definitely plays a multitudinous role.