• The Korean Journal of Physiology and Pharmacology
• /
• v.2 no.5
• /
• pp.573-580
• /
• 1998

The study aims to identify the mechanism (s) underlying the altered vasodilatory responses of the pial artery of spontaneously hypertensive rats (SHR) under a hypothesis that calcitonin gene-related peptide (CGRP) exerts a modulator role in the autoregulation of cerebral blood flow (CBF). The animals were divided into four groups: 1) Sprague-Dawley rats (SDR), 2) Wistar rats (WR), 3) SHR with high blood pressure $(BP{\ge}150\;mmHg),$ and 4) SHR with normotensive BP $({\le}150\;mmHg).$ The lower limit of CBF autoregulation in SHR shifted to a higher BP $(82.8{\pm}9.3\'mmHg,\;P<0.05)$ than that in SDR $(58.9{\pm}5.7\;mmHg)$. In SHR, whether the BP levels were high or normotensive, the vasodilator responses to a stepwise hypotension were significantly attenuated unlike with SDR and WR. When artificial cerebrospinal fluid (CSF) containing capsaicin $(3{\times}10^{-7}\;M)$ was suffused over the cortical surface, a transient increase in pial arterial diameter was observed in the SHR with high or normotensive BP. In contrast, SDR and WR showed a large increase in diameter, and the increase was sustained for over 10 minutes. In line with these results, the basal releases of CGRP-like immunoreactivity (CGRP-LI) in the isolated pial arteries from SHR with high and normotensive BP were $12.5{\pm}1.4\;and\;9.8{\pm}2.8\;fmole/mm^2/60\;min\;(P<0.05)$, while those from SDR and WR were $25.5{\pm}3.1\;and\;24.6{\pm}3.1\;fmole/mm^2/60\;min,$ respectively. The isolated basilar arteries showed similar results to those of the pial arteries in SHR. Thus, it is summarized that, in the SHR, the reduced autoregulatory vasodilator responses to stepwise hypotension and capsaicin may be, in part, ascribed to the decreased release of CGRP from the perivascular sensory nerve fibers of the pial arteries, and that altered vasomotor activity in SHR may not be related with the hypertensive tone.

• The Journal of Korean Obstetrics and Gynecology
• /
• v.20 no.2
• /
• pp.83-96
• /
• 2007

Purpose: Ligustri Lucidi Fructus and Ecliptae Herba has long been used for clinical therapy associated especially with menopausal symptoms in Korea. To provide a scientific rationale for such use, we have investigated the antioxidant and vasorelaxant effects of Ligustri Lucidi Fructus, Ecliptae Herba and its mixture. Methods: The antioxidant activity of the extracts from Ligustri Lucidi Fructus, Ecliptae Herba and its mixture were evaluated and compared with that of BHA (butylated hydroxyanisole), BHT (butylated hydroxytoluene), vitamin C and vitamin E, using the ${\alpha}$,${\alpha}-diphenyl-{\beta}-picrylhydrazyl$ (DPPH) radical scavenging method. Results: Antioxidant activity of all extracts using the DPPH radical scavenging method decreased in the order vitamin C>BHA>vitamin E>Ligustri Lucidi Fructus>Ligustri Lucidi Fructus:Ecliptae Herba(1:1)>Ecliptae Herba>BHT. The vasorelaxant effects of extracts were investigated on the vasomotor tone of the rat thoracic aorta in an organ bath. All of the extracts elicited along-term relaxing response in the endothelium-intact as well as endothelium-denuded rat aorta contracted with norepinephrine. This relaxant effect was abolished by Precontraction with 72 mM KCI. Thus, it is suggested that the mechanism of vasorelaxant effect of extracts not involve voltage-operated $Ca^{2+}$ channel blocking but receptor-mediated route. Conclusion: These antioxidant and vasorelaxant effecs of the extracts may contribute to the beneficial effects in postmenopausal women.

• The Korean Journal of Physiology
• /
• v.26 no.1
• /
• pp.75-88
• /
• 1992

It is well established that neurons in ventrolateral medulla play a key role in determining the vasomotor tone. The purpose of present study is to identify sympathetic related, medullospinal tract neurons in ventrolateral medulla and to show that these mediate somato-sympathetic reflex. Medullospinal tract cells were identified by antidromic stimulation to intermediolateral nucleus (IML) of the second thoracic ($T_2$) spinal cord in anesthetized cats. Peripheral nerves were stimulated for orthodromic activation of these cells and peripheral receptive fields were determined. Post R wave histogram of unit and spike triggered averaging of sympathetic nerve discharge (SND) were used to define sympathetic related cell. A total of 113 neurons was recorded in ventrolateral medulla that had the axonal projections to $T_2$ spinal cord. Thirty four of these medullospinal cells showed spontaneous discharges and the others not. Between these two groups, rostro-caudal coordinate of the distribution from obex [$4.7{\pm}0.2\;$ (mean S.E.) mm, 4.1 0.1 mm], depth from dorsal surface ($5.5{\pm}0.2mm,\;4.9{\pm}0.1mm$ and conduction velocity ($9.9{\pm}1.7m/sec,\;16.7{\pm}1.9\;m/sec$) were significantly different (p<0.05). In spontaneously discharging group, characteristics of rostral and caudal groups were significantly different and we demonstrated that cells in rostral group mediate somatosympathetic reflex. From these results, we conclude that a certain portion of spontaneously discharging medullospinal tract cells in rostral ventrolateral medulla comprise the efferent outputs of somatosympathetic reflex to sympathetic preganglion neurons.

• The Korean Journal of Physiology and Pharmacology
• /
• v.24 no.4
• /
• pp.287-298
• /
• 2020

Ca²⁺ signaling of endothelial cells plays a critical role in controlling blood flow and pressure in small arteries and arterioles. As the impairment of endothelial function is closely associated with cardiovascular diseases (e.g., atherosclerosis, stroke, and hypertension), endothelial Ca²⁺ signaling mechanisms have received substantial attention. Increases in endothelial intracellular Ca²⁺ concentrations promote the synthesis and release of endothelial-derived hyperpolarizing factors (EDHFs, e.g., nitric oxide, prostacyclin, or K⁺ efflux) or directly result in endothelial-dependent hyperpolarization (EDH). These physiological alterations modulate vascular contractility and cause marked vasodilation in resistance arteries. Transient receptor potential (TRP) channels are nonselective cation channels that are present in the endothelium, vascular smooth muscle cells, or perivascular/sensory nerves. TRP channels are activated by diverse stimuli and are considered key biological apparatuses for the Ca²⁺ influx-dependent regulation of vasomotor reactivity in resistance arteries. Ca²⁺-permeable TRP channels, which are primarily found at spatially restricted microdomains in endothelial cells (e.g., myoendothelial projections), have a large unitary or binary conductance and contribute to EDHFs or EDH-induced vasodilation in concert with the activation of intermediate/small conductance Ca²⁺-sensitive K⁺ channels. It is likely that endothelial TRP channel dysfunction is related to the dysregulation of endothelial Ca²⁺ signaling and in turn gives rise to vascular-related diseases such as hypertension. Thus, investigations on the role of Ca²⁺ dynamics via TRP channels in endothelial cells are required to further comprehend how vascular tone or perfusion pressure are regulated in normal and pathophysiological conditions.

• Journal of Chest Surgery
• /
• v.40 no.10
• /
• pp.701-703
• /
• 2007

Coronary artery vasospasm results in transient, abrupt chest pain that's due to the increased vasomotor tone of the coronary artery, and this can cause myocardial ischemia. We report here or one case of the right coronary artery vasospasm after aortic valve replacement surgery, and this was due to severe aortic regurgitation.

• The Korean Journal of Physiology and Pharmacology
• /
• v.2 no.3
• /
• pp.287-295
• /
• 1998

Diazepam is known to have cardiovascular depressive effects through a combined action on benzodiazepinergic receptor and the GABA receptor-chloride ion channel complex. Moreover, it is known that barbiturates also have some cardiovascular regulatory effects mediated by the central GABAergic system. Therefore, this study was undertaken to delineate the regulatory actions and interactions of these systems by measuring the responses of the cardiovascular system and renal nerve activity to muscimol, diazepam and pentobarbital, administered intracerebroventricularly in rabbits. When muscimol $(0.03{\sim}0.3\;{\mu}\;g/kg)$, diazepam $(10{\sim}100\;{\mu}\;g/kg)$ and pentobarbital $(1{\sim}10\;{\mu}\;g/kg)$ were injected into the lateral ventricle of the rabbit brain, there were similar dose-dependent decreases in blood pressure (BP) and renal nerve activity (RNA). The relative potency of the three drugs in decreasing BP and RNA was muscimol ＞ pentobarbital ＞ diazepam. Muscimol and pentobarbital also decreased the heart rate in a dose-dependent manner; however, diazepam produced a trivial, dose-independent decrease in heart rate. Diazepam $(30\;{\mu}g/kg)$ augmented the effect of muscimol $(0.1\;{\mu}g/kg)$ in decreasing blood pressure and renal nerve activity, but pentobarbital $(3\;{\mu}g/kg)$ did not. Bicuculline $(0.5\;{\mu}g/kg)$, a GABAergic receptor blocker, significantly attenuated the effect of muscimol in decreasing BP and RNA, either alone or with diazepam, and that of pentobarbital in decreasing BP and RNA, either alone or with muscimol. We inferred that the central benzodiazepinergic and barbiturate systems help regulate peripheral cardiovascular function by modulating the GABAergic system, which adjusts the output of the vasomotor center and hence controls peripheral sympathetic tone. Benzodiazepines more readily modulate the GABAergic system than barbiturates.

• Journal of Veterinary Clinics
• /
• v.27 no.3
• /
• pp.262-267
• /
• 2010

Magnesium ($Mg^{2+}$) is an essential co-factor for over 325 physiological and biochemical processes so that plays a central role of neuronal activity, cardiac excitability, neuromuscular transmission, muscular contraction, vasomotor tone, and blood pressure significantly related to physical performance. However, only limited information on blood ionized $Mg^{2+}$ ($iMg^{2+}$) regarding to physical exercise is available and the data from blood total $Mg^{2+}$ detection are inconsistent. This present study investigated the changes of blood $iMg^{2+}$ correlated with metabolic demands during acute high-intensive exhaustive physical exercise in rats. After exhausted swimming (3-4 hours), blood pH, glucose, $HCO_3{^-}$, oxygen and ionized $Ca^{2+}$ ($iCa^{2+}$) were significantly decreased, whereas lactate, carbon dioxide, $iMg^{2+}$, ionized $Na^+$ and ionized $K^+$ were significantly increased. During the exhausted swimming, the changes in $iMg^{2+}$ showed a significant negative correlation with changes in pH, glucose, $HCO_3^-$ and $iCa^{2+}$, however a significant negative correlation with changes in lactate and anionic gap. It is concluded that the acute high-intensive exhaustive physical exercise could produced hypermagnesemia, an increase in blood $iMg^{2+}$ via stimulation of $iMg^{2+}$ efflux following increase in intracellular $iMg^{2+}$ from muscle induced by metabolic and respiratory acidosis.

• Journal of Chest Surgery
• /
• v.39 no.12 s.269
• /
• pp.913-919
• /
• 2006

Background: Vasodilatory shock has been implicated in life-threatening complications after open heart surgery, where the systemic inflammatory reaction is attributed to the cardiopulmonary bypass(CPB). The secretion of arginine vasopressin(AVP) has been found to be defective in a variety of vasodilatory shock states and administration of AVP markedly improves vasomotor tone and blood pressure. So we reviewed our experience of AVP therapy in patients with vasodilatory shock following heart surgery using CPB. Material and Method: From January 2004 to July 2006, we reviewed the records of patients who received AVP therapy for vasodilatory shock following heart surgery using CPB. Vasodilatory shock was defined as a mean arterial pressure lower(MAP) than 70 mmHg, a cardiac index greater than 2.5 $L/min/m^2$, peripheral vascular resistance lower than 800 $dyn/s/cm^5$, and vasopressor requirements. The hemodynamic responses of patients who received AVP therapy for vasodilatory shock after cardiac surgery were analyzed retrospectively. Result: One hundred ninety nine open cardiac surgery patients were consecutively included in this study. Twenty two patients(11.1%) met criteria for vasodilatory shock. Despite the administration of high dose catecholamine vasopressor, all patients were hypotensive with a mean arterial pressure less than 70 mmHg. AVP therapy increased MAP from $53.3{\pm}7.4\;to\;82.0{\pm}12.0$ mmHg at 1 hour (p<0.001) and decreased other vasopressor requirements from $25{\pm}7\;to\;18{\pm}6$ at 1 hour(p<0.001) and individually maintained it for 12 hours. Conclusion: Our date suggest that AVP may be a safe and an effective vasopressor in patients with vasodilatory shock. In patients exhibiting vasodilatory shock after heart surgery, replacement of AVP increases blood pressure and reduces catecholamine vasopressor requirements.