• The Korean Journal of Physiology
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• 제23권1호
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• pp.67-78
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• 1989

Since the atrial receptor was suggested to be involved in the control of extracellular fluid volume, it has been shown that the granularity of atrial cardiocytes can be changed by water and salt depletion, and that an extract of atrial tissue, when injected intravenously into anesthetized rats, causes a large and rapid increase in renal excretions of sodium and water. The immunoreactive atrial natriuretic peptide (ANP) has been found in the plasma of patients suffering from various cardiovascular diseases. A high level of ANP in the plasma has been reported in essential hypertension. Several studies on the effects of ANP on renal function and arterial blood pressure have presented contradictory results showing attenuated or accentuated responses. Thus, involvement of the ANP in the development of hypertension remains unresolved. Present study was undertaken to investigate whether the ANP is involved in the development of hypertension in two-kidney one-clip Goldblatt hypertensive rats. The plasma concentration of immunoreactive ANP appeared to be significantly elevated in hypertensive rats as compared with normotensive Goldblatt operated and sham-operated rats. Plasma renin concentration was higher in hypertensive rats than in normotensive rats, as observed in earlier experiments. Intravenous infusions of ANP resulted in increases of urine flow and urinary excretions of sodium and potassium in both hypertensive and normotensive rats. The renal response to ANP was markedly accentuated in Goldblatt hypertensive rats. The plasma concentration of ANP showed a linear relationship with the arterial blood pressure. Infusions of ANP reduced blood pressure both in hypertensive and normotensive rats. These results suggest that in Goldblatt hypertensive rats an elevation of ANP level in the plasma may not be a cause, but instead a consequence of hypertension, and that the renal responsiveness to the ANP is accentuated by some unknown mechanisms.

• The Korean Journal of Physiology
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• 제20권1호
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• pp.89-102
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• 1986

It has long been suggested that the change of renin-angiotensin system is responsible for the increased arterial blood pressure in the experimental hypertension. But the exact nature of the cause and maintenance of early and late Phase of renal hypertension is still controversial. Increased renin-angiotensin system has been suggested. To clarify the altered renin-angiotensin system in the early phase of two kidney one clip Goldblatt hypertension(2K1C GH), experiments were carried out in the rats of 3,7, and 14 days of 2K1C GH rats, sham-operated, and control rats. Responses of the plasma renin activity to the intravenous infusion of L-isoproterenol were dose-dependent. Responses of the plasma renin activity to the intravenous L-isoproterenol in 2K1C GH rats were not different from sham-operated control rats. Hypotensive responses of the 2K1C GH rats were not different from sham-operated rats. Suppression by intravenous infusion of angiotensin II of plasma renin activity showed a dose-dependent manner. Suppression by angiotensin ll of plasma renin activity was attenuated or abolished in the early phase of 2K1C GH rats. Intravenous infusion of arginine vasopressin(AVP) showed a dose-dependent suppression of plasma renin activity, Attenuated responses by AVP of plasma renin activity were noticed in the early phase of 2K1C GH rats. These results suggest that the altered renin-angiotensin system in the early phase of the two kidney one clip Goldblatt hypertension may be caused by failure of the short loop negative feedback control mechanism.

• Journal of Acupuncture Research
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• 제21권4호
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• pp.1-18
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• 2004

Objective : This study was performed to investigate the effects of aqua-acupuncture of Jibaikjihwangtang in two-kidney one clip Goldblatt hypertensive rats and spontaneously hypertensive rats. Methods : we injected aqua-acupuncture solution into Shin-Soo ($BL_{23}$) which corresponds to human acupuncture point in two-kidney one clip Goldblatt hypertensive rats and spontaneously hypertensive rats. Systolic blood pressure, renin activity, aldosterone and atrial natriuretic peptide (ANP) plasma levels were tested. Results : Systolic blood pressure decreased significantly after aqua-acupuncture of jibaikjihwangtang. Acupuncture group in two-kidney one clip Goldblatt hyper-tensive rats had deference with control group. In plasma levels of atrial natriuretic peptide, acupuncture group of spontaneously hypertensive rats increased meaningfully but to two-kidney one clip Goldblatt hypertensive rats it was decreased meaningfully. In Serum Aldosterone density, the acupuncture group of spontaneously hypertensive rats had significant alteration than control group, but the acupuncture group of two-kidney one clip Goldblatt hypertensive rats had decreased alteration than control group. Conclusion : According to these results, after Aqua-Acupuncture of Jibaikjihwangtang blood pressure decreased significantly and data suggest that blood pressure reduction activity connected with renin activity reduction in renal hypertensive rat.

• The Korean Journal of Physiology
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• 제20권2호
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• pp.236-248
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• 1986

Alterations of renin-angiotensin system have been suggested as one of the mechanisms increasing arterial blood pressure in experimental and clinical hypertension. But the exact nature of high blood pressure in the early and late phase of renal hypertension is still controversial. To clarify the nature of renin release in both unclipped and clipped kidney of two kidney one clip Goldblatt lypertensive rat, experiments have been done in kidney slices, which were obtained from the rats of 3 and 7 days of operation. Basal rate of renin release was suppressed in unclipped kidney slices compared to clipped kidney Norepinephrine increased renin release from unclipped kidney slices, but not from clipped kidney slices. Suppressions by angiotensin Il and arginine vasopressin of renin release were attenuated in the clipped kidney slices compared to unclipped and sham-operated kidney slices. Increases by verapamil and trifluoperazine of renin release were attenuated in the clipped kidney slices compared to unclipped and sham-operated kidney slices. These results suggest that the negative feedback control mechanism of the renin-angiotensin system by angiotensin Il and arginine vasopressin is attenuated in the clipped kidney of two kidney one clip Goldblatt hypertensive rat, and that one of the altered mechanisms may be caused by certain regulatory changes of intracellular calcium and/or calcium-calmodulin complex in the juxtaglomerular cells.

• The Korean Journal of Physiology
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• 제28권2호
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• pp.191-196
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• 1994

Captopril, an inhibitor of angiotensin converting enzyme, is also known to inhibit the degradation of bradykinin. We examined the effects of intracerebroventricular (ICV) captopril on the central pressor response to bradykinin in normotensive, 2-kidney, 1 clip Goldblatt (GHR) and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Captopril (1 mg) and bradykinin (5 nmol) were administered into the right lateral cerebral ventricle, and blood pressure and heart rate were continuously monitored throughout the experiment. ICV captopril alone did not affect the blood pressure within 10 minutes but it significantly augmented the central pressor response to bradykinin in GHR. On the contrary, captopril was without effect on the pressor response to bradykinin in normotensive and DOCA-salt rats. These findings indicate that endogenous kinins are not critical in regulating arterial pressure in normotensive and DOCA hypertensive rats. However, in GHR, an enhanced activity of the brain kallikrein-kinin system in maintaining the high blood pressure is suggested.

• The Korean Journal of Physiology and Pharmacology
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• 제3권5호
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• pp.471-479
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• 1999

The Kv channel activity in vascular smooth muscle cell plays an important role in the regulation of membrane potential and blood vessel tone. It was postulated that increased blood vessel tone in hypertension was associated with alteration of Kv channel and membrane potential. Therefore, using whole cell mode of patch-clamp technique, the membrane potential and the 4-AP-sensitive Kv current in cerebral arterial smooth muscle cells were compared between normotensive rat and one-kidney, one-clip Goldblatt hypertensive rat (lK,lC-GBH rat). Cell capacitance of hypertensive rat was similar to that of normotensive rat. Cell capacitance of normotensive rat and 1K,lC-GBH rat were $20.8{\pm}2.3$ and $19.5{\pm}1.4$ pF, respectively. The resting membrane potentials measured in current clamp mode from normotensive rat and 1K,lC-GBH rat were $-45.9{\pm}1.7$ and $-38.5{\pm}1.6$ mV, respectively. 4-AP (5 mM) caused the resting membrane potential hypopolarize but charybdotoxin $(0.1\;{\mu}M)$ did not cause any change of membrane potential. Component of 4-AP-sensitive Kv current was smaller in 1K,lC-GBH rat than in normotensive rat. The voltage dependence of steady-state activation and inactivation of Kv channel determined by using double-pulse protocol showed no significant difference. These results suggest that 4-AP-sensitive Kv channels playa major role in the regulation of membrane potential in cerebral arterial smooth muscle cells and alterations of 4-AP-sensitive Kv channels would contribute to hypopolarization of membrane potential in 1K,lC-GBH rat.

• The Korean Journal of Physiology
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• 제30권2호
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• pp.269-278
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• 1996

The mechanism of impaired endothelium-dependent relaxation in the aorta of one-kidney, one clip Goldblatt hypertensive (1K,1C-GBH) rats was investigated. 8 week-old Wistar-Kyoto (WKY) rats were made hypertensive by left renal artery stenosis with contralateral nephrectomy. Endothelium-dependent relaxation was significantly reduced in 1K,1C-GBH rats as compared with WKY rats. However, the relaxation by sodium nitroprusside in 1K,1C-GBH rats was not reduced as compared with WKY rats. The impairment of endothelium-dependent relaxation in 1K,1C-GBH rats was partially restored by the pretreatment of indomethacin or SQ29548. When the nitric oxide production was inhibited by L-nitroarginine methyl ester, acetylcholine (ACh) induced a endothelium-dependent contraction that was greater in 1K,1C-GBH rats than in WKY rats. Endothelium-dependent contraction by ACh was completely abolished by indomethacin or SQ29548. However, imidazole, tranylcypromine and superoxide dismutase did not affect the endothelium-dependent contraction in 1K,1C-GBH rats. These results suggest that impaired endothelium-dependent relaxation in the 1K,1C-GBH rats might be due to the simultaneous release of EDCF, and that prostaglandin B2 may be involved as a mediator of endothelium-dependent contraction.

• The Korean Journal of Physiology
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• 제26권1호
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• pp.69-74
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• 1992

Central cardiovascular effects of bradykinin were examined in anesthetized normotensive (NTR) and 2-kidney, 1 clip Goldblatt hypertensive rats (GHR). Bradykinin ($0.5{\sim}10nmol$) was administered into the right lateral cerebral ventricle, while blood pressure and heart rate (HR) were continuously monitored. In both NTR and GHR, intracerebroventricular bradykinin produced a dose dependent increase in mean arterial pressure (MAP) without significant changes in HR. GHR were more sensitive in the pressor response than NTR. The pressor response to bradykinin was attenuated by treatment with hexamethonium (2.5mg/kg/min, IV) or phentolamine (2mg/kg, IV) in both NTR and GHR. Reserpine treatment (2mg/kg/day, intramuscularly,2 days) did not affect the central pressor effect of bradykinin in NTR but it attenuated the pressor effect in GHR. Pretreatment with indomethacin (10mg/kg, intraperitoneally) or saralasin ($20{\mu}g$/kg/min, IV) was without effects on the pressor response to bradykinin. These results indicate that the central pressor effect of bradykinin is, at least in part, due to excitation of the autonomic nervous activity. Mechanisms other than the enhanced sympathetic nervous activity ran. not be ruled out, However. It is also suggested that the sensitivity to bradykinin is increased in the GHR.

• The Korean Journal of Physiology
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• 제16권1호
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• pp.63-68
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• 1982

The change of plasma renin activity is one of the most important parameters explaining the pathological physiology of the hypertension. The relation between renal renin activity and plasma renin activity has not well been documented since last decades. In an attempt to clarify the relationship a series of experiments have been done in rats. The following results were observed. 1) Renal renin activity of clamped kidney increased after silver clipping and the increments were maintained until four to five weeks of operation. 2) Renal renin activity of the untouched contralateral kidney was vulnerable to be suppressed just after clamping, and the activity disappered almost below the limitation of the radioimmunoassay sensitivity up to four weeks. 3) Plasma lenin activity was changed by the renal renin activity, but the regression coefficient from the two kidney one clip Goldblatt hypertensive rats was different from the sham-operated, or age-matched control rats. 4) Plasma renin activity of all the groups tested has the exponential curve in terms of renal renin activity. These data suggest that the renal renin activity is important to control the plasma renin activity in certain experimental condition, especially in chronic status.

• The Korean Journal of Physiology
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• 제23권1호
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• pp.43-49
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• 1989

Atrial natriuretic peptide (ANP)의 혈압조절에 대한 효과를 구명하기 위하여 2-kidney, 1-clip 흰쥐의 고혈압 발생에 미치는 ANP의 영향을 조사하였다. 실험군은 왼쪽 신동맥에 clip을 끼우고 경정맥내에 지속적으로 ANP를 주입한(atriopeptin III, 500 ng/h) 군으로 하였으며, 대조군은 clip을 끼웠으나 ANP를 주입하지 않은 군으로 하였다. Clip을 끼우기 전과 clip을 끼운 제 4,7,10일에 꼬리동맥으로부터 혈압을 측정한 후 단두하여 혈액을 채취하고 양측 신장을 떼어내어 renin 치를 구하였다. ANP 주입군은 대조군에 비하여 고혈압의 발생이 약화되었고 혈장 renin활성도가 유의하게 낮았으나 신피질 renin함량은 양군간에 유의한 차이가 없었다. 한편 clip을 끼우지 않은 흰쥐에서는 ANP 주입군과 비주입군간에 혈압, 혈장 renin 활성도와 신피질 renin 함량 등이 모두 서로 유의한 차이를 보이지 않았다. 이상의 실험결과는 지속적 ANP 주입이 2-K, 1-C 흰쥐의 고혈압 발생을 방지하지는 못하였으나 약화시켰음을 보여주었으며, ANP는 적어도 부분적으로는 renin-angiotensin계를 길항하므로써 장기적 혈압 조절에 관여하는 것이 시사되었다.