Systemic capsaicin treatment impairs the micturition reflex in the rat

Holzer‐Petsche, Ulrike; Lembeck, Fred

doi:10.1111/j.1476-5381.1984.tb16534.x

Cited by 125 publications

(33 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On the first and second days of life, neonatal rats received 50 mg/kg SC capsaicin as described. 15,16 Control rats were treated with equal volumes of vehicle solution (5% ethanol, 5% Tween-80 in saline). All treatments were performed with rats under ether anesthesia.…”

Section: Animal Groupsmentioning

confidence: 99%

Development of Hypertension Induced by Subpressor Infusion of Angiotensin II

Zhang

Ballew

et al. 2000

Hypertension

View full text Add to dashboard Cite

Abstract-Long-term administration of a subpressor dose of angiotensin II (Ang II) leads to pressor hyperresponsiveness and slow development of hypertension. Our preliminary data show that mRNA expression for calcitonin-gene related peptide in dorsal root ganglia was significantly increased by subpressor infusion of Ang II. To determine the role of sensory nerves in the development of hypertension induced by subpressor infusion of Ang II, newborn Wistar rats were given 50 mg/kg SC capsaicin on the 1st and 2nd days of life. After the weaning period, male rats were divided into 4 groups and subjected to the following treatments for 2 weeks: capsaicinϩAng II (150 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 SC by osmotic pumps, CAP-AII), capsaicinϩvehicle (CAP), controlϩAng II (CON-AII), and controlϩvehicle (CON). The results show that mean arterial pressure was significantly elevated in both Ang II-infused rats compared with non-Ang II-treated rats (PϽ0.05), and it was higher in CAP-AII than in CON-AII rats (PϽ0.05). The 24-hour urinary and sodium excretions were lower in CAP-AII than in CON-AII, CAP, and CON rats (PϽ0.05). These data demonstrated that sensory denervation exacerbates the development of hypertension and impairs renal excretory function when a subpressor dose of Ang II is given. These results indicate that activation of sensory nerves, either by Ang II or by other hormonal or hemodynamic factors, plays a compensatory role in promoting urine and sodium excretion and attenuating elevated blood pressure initiated by Ang II. (Hypertension. 2000;36:549-552.) Key Words: Angiotensin II Ⅲ peptides Ⅲ hypertension, experimental I t is now clear that acute elevation of blood pressure induced by administration of pressor doses of Angiotensin (Ang) II is mainly caused by increased aldosterone production, salt and water retention, and resetting of the baroreceptor that results in increased sympathetic tone. [1][2][3][4][5][6] In addition, acute elevation of blood pressure has been shown to trigger compensatory mechanisms, for example, natriuresis and the local production of prostaglandins, 7,8 which may attenuate the increase in blood pressure induced by pressor doses of Ang II. In contrast, the slow development of hypertension induced by long-term administration of subpressor doses of Ang II mimics the development of human hypertension to a greater extent than the administration of pressor doses. During the developmental stage of hypertension, altered aldosterone levels and salt and water retention cannot be detected. 8 -12 Although intensive research has been conducted in this area, mechanisms underlying subpressor Ang II-induced hypertension are largely unknown.There is evidence showing that the renin-angiotensin system interacts with sensory nerves to modulate cardiovascular function. 13 Sensory afferent nerves have cell bodies located in the dorsal root ganglia (DRG) and extend their processes to a variety of tissues including renal tubules, resistance arteries, and heart. It has been established that sensory afferent fibers releas...

show abstract

Section: Animal Groupsmentioning

confidence: 99%

Development of Hypertension Induced by Subpressor Infusion of Angiotensin II

Zhang

Ballew

et al. 2000

Hypertension

View full text Add to dashboard Cite

show abstract

“…On days 1 and 2 of life, neonatal rats received capsaicin 50 mg/kg SC as described. 2,8,9 Control rats were treated with equal volumes of vehicle solution (5% ethanol, 5% Tween 80 in saline). All treatments were performed with rats under ether anesthesia.…”

Section: Animalsmentioning

confidence: 99%

Antihypertensive Mechanisms Underlying a Novel Salt-Sensitive Hypertensive Model Induced by Sensory Denervation

Wang

1999

Hypertension

View full text Add to dashboard Cite

Abstract-A novel model of hypertension recently developed in our laboratory shows that neonatal degeneration of capsaicin-sensitive sensory nerves renders a rat responsive to a salt load with a significant rise in blood pressure. To determine the role of the renin-angiotensin system and the sympathetic nervous system in the development of hypertension in this model, newborn Wistar rats were given capsaicin 50 mg/kg SC on the first and second days of life. Control rats were treated with vehicle. After they were weaned, male rats were divided into 6 groups and subjected to the following treatments for 2 weeks: controlϩhigh sodium diet (4%) (CON-HS), capsaicinϩnormal sodium diet (0.5%) (CAP-NS), capsaicinϩhigh sodium diet (CAP-HS), capsaicinϩhigh sodium dietϩlosartan (10 mg/kg per day) (CAP-HS-LO), capsaicinϩhigh sodium dietϩprazosin (3 mg/kg per day) (CAP-HS-PR), and capsaicinϩhigh sodium dietϩhydralazine (10 mg/kg per day) (CAP-HS-HY). Levels of calcitonin gene-related peptide in dorsal root ganglia were decreased by capsaicin treatment (PϽ0.05). Both tail-cuff systolic blood pressure and mean arterial pressure were higher in CAP-HS and CAP-HS-PR than in CON-HS, CAP-NS, CAP-HS-LO, and CAP-HS-HY (PϽ0.05). The 24-hour urinary volume and sodium excretion were increased when a high sodium diet was given (PϽ0.05), but they were lower in CAP-HS, CAP-HS-LO, CAP-HS-PR, and CAP-HS-HY than in CON-HS (PϽ0.05). Urinary potassium excretion was not different among all 6 groups. We conclude that blockade of the angiotensin type 1 receptor with losartan but not antagonism of the ␣ 1 -adrenoreceptor with prazosin prevents the development of salt-sensitive hypertension induced by sensory denervation. Sensory denervation impairs urinary sodium and water excretion in response to a high sodium intake, regardless of blood pressure, suggesting that sensory innervation plays a direct role in regulating the natriuretic response to sodium loading. Key Words: capsaicin Ⅲ sodium, dietary Ⅲ innervation, sensory Ⅲ hypertension, salt-sensitive Ⅲ renal circulation I t is well established that in a considerable number of essential hypertensive patients and patients with glomerulonephritis, primary aldosteronism, and diabetes mellitus, blood pressure is sodium sensitive. 1 Despite intensive research in this area, the cellular and molecular mechanisms underlying salt-sensitive hypertension are not well defined, and no pharmacological approaches have been developed that directly target the defect in salt handling. The existing genetic and experimental animal models of salt-sensitive hypertension, eg, Dahl salt-sensitive rats, Milan hypertensive rats, and deoxycorticosterone-salt hypertensive rats, have been widely used to explore underlying mechanisms linked to saltsensitive hypertension. 1 Recently, we developed a novel salt-sensitive hypertensive model that is sensory nerve dependent. We found that capsaicin-induced degeneration of sensory nerves in rats impairs normal increase in urinary sodium and water excretion when a high sodium diet is give...

show abstract

“…On the first and second days of life, neonatal rats received capsaicin, 50 mg/kg s.c., as described. 1,2,7,8 Control rats were treated with equal volumes of vehicle solution (5% ethanol, 5% Tewwn 80 in saline). After three weeks, male rats were divided into four groups, pair-fed different sodium diets, and subjected to following treatments for three weeks: control + high sodium diet (4%, CON-HS), capsaicin pretreatment + normal sodium diet (0.5%, CAP-NS), capsaicin pretreatment + high sodium diet (CAP-HS), capsaicin pretreatment + high sodium diet + candesartan cilexetil (10 mg/kg/per day by oral gavage) (CAP-HS-CAN).…”

Section: Animalsmentioning

confidence: 99%

Development of salt-sensitive hypertension in a sensory denervated model: the underlying mechanisms

Wang

Huang

2001

J Renin Angiotensin Aldosterone Syst

View full text Add to dashboard Cite

We use a novel salt-sensitive hypertensive model recently developed in our laboratory. This model shows that neonatal degeneration of capsaicin-sensitive sensory nerves renders a rat responsive to a salt load with a significant rise in blood pressure (BP). To test the hypothesis that development of salt-sensitive hypertension in sensory denervated rats is mediated by abnormal regulation of both circulating and tissue renin-angiotensin systems (RAS), neonatal Wistar rats were given capsaicin, 50 mg/kg s.c., on the first and second days of life. Control rats were treated with vehicle solution. After the weaning period, male rats were divided into four groups and subjected to the following treatments for three weeks: control + high sodium diet (

show abstract

Systemic capsaicin treatment impairs the micturition reflex in the rat

Cited by 125 publications

References 31 publications

Development of Hypertension Induced by Subpressor Infusion of Angiotensin II

Development of Hypertension Induced by Subpressor Infusion of Angiotensin II

Antihypertensive Mechanisms Underlying a Novel Salt-Sensitive Hypertensive Model Induced by Sensory Denervation

Development of salt-sensitive hypertension in a sensory denervated model: the underlying mechanisms

Contact Info

Product

Resources

About