| Capsaicin (8-methyl-6-nonenamide), the major pungent ingredient of hot chilli peppers,excites a subset of primary afferent neurons.The Hungarian pharmacologist Nicholas Jancso began an extensive characterization of the pharmacological effects of capsaicin in the late 1940s. A large body of studies have demonstrated that capsaicin can activate the nociceptive sensory neurons with C and Aδfibers and its effects are mediated through vanilloid receptor subtype 1(VR1). Previous studies have shown the different effects of capsaicin on cardiovascular system elicited after peripheral or central administration. Since the baroreceptor and baroreflex play a major role in the maintainence of blood pressure and the effect of capsaicin on carotid sinus baroreceptor activity and baroreflex have not been reported yet, the goals of the present research were to observe: ⑴ effect of capsaicin on carotid sinus baroreflex in anesthetized rat, and ⑵ effect of capsaicin on carotid sinus baroreceptor activity in anesthetized rats. The results are as follows:1 Capsaicin facilitates carotid sinus baroreflex in anesthetized rat The effects of capsaicin (CAP) on the carotid sinus baroreflex were studied in 30 anaesthetized rats with perfused isolated carotid sinus. The results are as follows. (1) By perfusing the isolated carotid sinus with CAP (1μmol/L), the functional curve of the baroreflex was shifted to the left and downward, with a peak slope (PS) increasing from 0.34 ± 0.01 to 0.42 ± 0.01 (P < 0.01), whereas the reflex decrease in mean arterial pressure (RD) was enhanced from 36.51 ± 1.26 to 45.01 ± 0.71 mmHg (P < 0.01). Meanwhile, the threshold pressure (TP), equilibrium pressure (EP) and saturation pressure (SP) were all significantly decreased from 70.43 ± 2.09 to 52.86 ± 2.80 mmHg (P < 0.01), 95.5 ± 1.71 to 87.00 ± 1.58 mmHg (P < 0.01) and 177.60 ± 1.37 to 163.55 ± 2.12 mmHg (P < 0.01), respectively. Among the functional parameters of carotid baroreflex, the changes in PS and RD induced by capsaicin were dose-dependent. (2) By pretreatment with ruthenium red (RR, 100 μmol/L), an antagonist of vanilloid receptor subtype 1 (VR1), the above effects of CAP on carotid baroreflex were abolished. (3) The CAP-induced change in the baroreflex was also eliminated by pretreatment with glibenclamide (20 μmol/L), a KATP channel blocker. On the basis of the results, it is concluded that CAP facilitates the carotid baroreflex, an effect of which may be resulted from the opening of KATP channels mediated by VR1.Key words: capsaicin; ruthenium red; glibenclamide; baroreflex 2 Capsaicin facilitates carotid sinus baroreceptor activity in anesthetized ratsThe effects of capsaicin (CAP) on the carotid sinus barorereceptor activity were studied in 30 anaesthetized rats with perfused isolated carotid sinus. The results are as follows. (1) Low-concentration of capsaicin (0.2 μmol/L) had no significant effect on CBA, while perfusion the isolated carotid sinus with middle-concentration of capsaicin (1 μmol/L) could shift FCCB to the left and upward, with peak slope (PS) increased from (2.47±0.14) %/mmHg to (2.88±0.10)%/mmHg (P<0.05) and peak integral value of carotid sinus nerve discharge (PIV) enhanced from (211±5.13)% to (238±6.03)% (P<0.01), and the threshold pressure (TP) , saturation pressure (SP) were significantly decreased from 68.0±1.06 to 62.7±1.03 mmHg (P<0.01) and from 171±1.61 to 165±0.61 mmHg (P<0.01). By perfusing with high-concentration of capsaicin (5 μmol/L), FCCB was shifted to the left and upward further and the changes of the functional parameters such as PS, TP and SP were concentration-dependent. (2) Pretreatment with ruthenium red (100 μmol/L), an antagonist of vanilloid receptor subtype 1 (VR1), blocked the effect of capsaicin on CBA. (3) Preperfusion with glibenclamide (20 μmol/L), a KATP channel blocker, could eliminate the effect of capsaicin on CBA. In summary, capsaicin exerts a facilitatory role on the isolated carotid baroreceptor in a concentration-dependent manner. The facili...
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