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Abstract

Formation of nitric oxide, and endothelium-derived relaxing factor, can be inhibited by administration of N-nitro-L-arginine methylesther (L-NAME). In the present study, the activity of the sympathoadrenal system in rats with blood pressure (BP) elevation induced by L-NAME was investigated. L-NAME was administered in a dose of 50 mg/kg, i.p. every 12 h for 4 days. Blood samples were collected via chronically inserted arterial catheters in conscious, freely moving rats at rest and during immobilization stress. Plasma epinephrine (EPI), norepinephrine (NE), and dopamine (DA), as well as catecholamine metabolites dihydroxyphenylglycol (DHPG) and dihydroxyphenylacetic acid (DOPAC) were measured by HPLC method. In L-NAME treated animals, which slowed a significant increase in BP, plasma EPI levels were markedly elevated both before and during stress. Plasma NE levels were not significantly increased, however, DHPG levels, which indicate NE turnover and reuptake, were highly elevated. Plasma DA levels were not changed after L-NAME administration but DA metabolite DOPAC showed a significant elevation both under basal conditions and during stress. Thus, the present results indicate that the prolonged blockade of nitric oxide synthesis that causes arterial hypertension is associated with an activation of the sympathoadrenal system.

Fractionation and bioassay-guided isolation of antihypertensive components of Senecio serratuloides

“…In line with the fact that L-NAME upregulates NE release and metabolism, the bioactive compounds and some sub-fractions that decreased BP may have acted as adrenergic antagonists or they had the ability to decrease interstitial NE concentration. Decreased heart rates induced by L-NAME were consistent with previous studies (Fellet et al, 2003;Kvetnansky et al, 1997).…”

“…From this proposal it is possible that decreased HR induced by L-NAME maybe as a result of activation of baroreceptor afferents by increased BP which resulted in activation of the parasympathetic vagal innervations of the heart. Considering the second suggestion, a study done by Kvetnansky et al (1997) revealed significant elevation of NE metabolites in L-NAME treated animals in spite of unchanged levels of plasma NE thus suggesting that L-NAME increases release, turnover, reuptake and metabolism of NE in the sympathoneural system. In line with this suggestion, Saeed, Khan, & Shabbir (2012) found that the magnitude of interstitial NE can increase far greater than that in plasma and thus they suggested that NE movement into the circulation decreases with baroreceptor unloading.…”

Anti-Hypertensive Activity of Some Selected Unani Formulations: An Evidence-Based Approach for Verification of Traditional Unani Claims Using LC-MS/MS for the Evaluation of Clinically Relevant Blood Parameters in Laboratory Rats

“…The adrenergic activation by L-NAME leads to the release of adrenaline and Noradrenaline, eventually exerting positive inotropic and chronotropic effect on the myocardium causing elevated blood pressure. It also acts by increasing Renin and Ang-II levels in the renal system, thereby augmenting plasma aldosterone and retaining Na + and water [ 17 ].…”

Role of Nitric Oxide in the Cardiovascular and Renal Systems

“…As mentioned earlier, the absence of NO can heighten the vasoconstriction phenomenon by increasing the levels of vasoconstrictors like NA and Ang II. This point could be explained by a prolonged blockade of nitric oxide synthesis that causes arterial hypertension (associated with an activation of the sympathoadrenal system) [ 142 ]. Nitric oxide is not only involved in functional antagonism of NA, but also affects the production of NA.…”