Biomedical subjects

A Gairard

Publications and source records attributed to A Gairard.

At least 19 recordsLinked to original sources

PubMed2001

Maturation reveals a decrease in endothelium-dependent contraction induced by depolarization in the aorta of spontaneously hypertensive rats.

The influence of the endothelium on aortic contractility to KCl 100 mM was studied during maturation and aging in normotensive Wistar and spontaneously hypertensive rats (SHR). In Wistar rats, there was no significant difference in maximal responses in the course of aging whether the endothelium was present (E+) or not (E-). A similar result was obtained in SHR E- rings. However, contraction was significantly higher in E+ rings of young (9 weeks) compared to adult and old SHR (18, 25, 36 and 72 weeks) (in mN/mm2: 34.8 +/- 3.1 versus 24.8 +/- 1.8, 16.0 +/- 2.5, 17.4 +/- 2.0 and 12.9 +/- 1.8, p<0.01). This increase remained significant in 18- compared to that of 25-, 36- and 72-week-old rats (p<0.01). No change appeared with age in noradrenaline-induced contractions of E+ rings neither in Wistar nor in SHR. A dose-dependent decrease in response to KCl was observed after an in vivo pretreatment of the young SHR with acetylsalicylic acid. Finally, blocking the TXA2/PGH2 receptor by addition of GR 32191B or ONO-3708 led to a decrease in the response of young SHR aortic rings to KCl. This study points out a decrease in the response of SHR aortic rings to a depolarizing agent during maturation. The enhanced contraction observed in young SHR seems to be the result of an increased participation of an endothelium-derived, cyclooxygenase-dependent contracting factor(s), most likely either TXA2 or PGH2. This factor might play a key role in the onset of hypertension in the spontaneously hypertensive strain.

Aging↗

PubMed2001

Hypotensive effect of endothelin-1 in nitric oxide-deprived, hypertensive pregnant rats.

Both nitric oxide (NO) and endothelin-1 (ET-1) are important mediators in the regulation of vascular tone during pregnancy and preeclampsia. This study was designed to investigate the ET-1-induced hypotensive effect in late pregnant rats (P) and in NO-deprived hypertensive pregnant rats (TP), a model of preeclampsia. From day 13 of pregnancy Wistar rats were fed a control or an N(omega)-nitro-L-arginine-enriched diet. On gestational day 20, mean arterial pressure (MAP +/- SEM, in mm Hg) and heart rate (HR) were measured with a carotid catheter in anesthetized rats after a bolus intravenous injection of several agonists and antagonists. After 7 days of chronic NO synthase inhibition, there was a significant increase in MAP (+45 +/- 3.9, P < .01) and 24-h urinary nitrate excretion was significantly decreased (P < .05). ET-1 bolus injection (0.1 nmol/kg) was rapidly followed by a significant decrease in MAP and a slight delayed increase, with no change in HR. The magnitude of the decrease had significantly dropped off in P (-30 +/- 2.2) as compared to that in TP (-46 +/- 5.1) and in virgin rats (-51 +/- 6.3) (P < .05). In P and TP, in vivo depressor effect was also obtained with sarafotoxin S6c, a specific ETB agonist, and blocked by the specific ETB antagonist BQ-788. After inhibition of cyclooxygenase with acetylsalicylic acid, the ET-1-induced hypotension was not modified either in P or in TP. In conclusion, the present data highlight an enhanced ETB receptor mediated hypotensive effect of ET-1 in anesthetized TP as compared to P. The magnitude of the hypotensive effect of ET-1 observed in TP is of the same order as that in virgin rats and neither NO nor vasodilator prostaglandins seem to be involved in TP. The enhanced hypotensive effect of ET-1 could be a beneficial counter-balancing mechanism in this rat model of preeclamptic pathology where an increased sensitivity to vasoconstrictor agents is generally described.

Animals↗

PubMed2000

Monitoring plasma levels of ganciclovir in AIDS patients receiving oral ganciclovir as maintenance therapy for CMV retinitis.

OBJECTIVES: To investigate whether low ganciclovir serum levels in patients on maintenance oral ganciclovir therapy are associated with recurrence of CMV retinitis. METHODS: A prospective study of the plasma concentration of ganciclovir after initiation of maintenance oral ganciclovir therapy in 14 AIDS patients who had recovered from acute cytomegalovirus (CMV) retinitis. RESULTS: Five of the 14 patients exhibited a mean time to recurrence of 37 days. The mean trough plasma concentration of ganciclovir in these patients after 1 month of oral ganciclovir therapy, was 0.40 +/- 0.30 mg/L. Nine patients had a mean time of progression of 263 days. The mean trough plasma concentration of ganciclovir in the latter patients was 0.80 +/- 0.60 mg/L. CONCLUSIONS: Patients exhibiting trough plasma levels of ganciclovir below 0.6 mg/L may be at higher risk of progression than patients who exhibited levels above 0.6 mg/L.

AIDS-Related Opportunistic Infections↗

PubMed2000

Endothelium and aortic contraction to endothelin-1 in the pregnant rat.

Endothelium-derived factors modulate tone and may be involved in hyporeactivity to vasoconstrictors, such as norepinephrine or angiotensin II, as has been previously described during gestation. The endothelium produces endothelin-1, a major vasoconstrictor peptide, therefore aortic contractions to endothelin-1 (10(-10) to 3 x 10(-7) M) were used to assess the role of the endothelium in pregnant Wistar rats (at 20 days of gestation). Late pregnancy is characterized by a significantly diminished systolic blood pressure in conscious rats (-17 mmHg, P < 0.001, n = 14). In pregnant and in age-matched nonpregnant female rats, endothelin-1 induced aortic contraction was greater when endothelium was present (at least P < 0.01). Indomethacin significantly reduced this contraction in aortic rings with intact endothelium in all groups. In aortic rings that had endothelium physically removed, contraction to endothelin-1 was greater in pregnant rats than in nonpregnant ones. Indomethacin decreased contraction of aortic rings in pregnant rats only. These results suggest an enhanced synthesis of vasoconstrictors by cyclooxygenases in vascular smooth muscle during pregnancy. In vessels with intact endothelium, we did not find hyporeactivity to endothelin-1 during late pregnancy. Contraction to endothelin-1 involved ET(A) receptors because it was decreased by BQ-123, an ET(A) receptor antagonist, whereas there was no significant change when using BQ-788, an ET(B) receptor antagonist.

Animals↗

PubMed1999

Endothelin-1 and relaxation of the rat aorta during pregnancy in nitroarginine-induced hypertension.

In pregnant rats during hypertension induced by NO synthase inhibition, endothelin (ET) plasma levels are increased as in some preeclamptic women. Previously, the enhanced vasodepressor effect of endothelin-1 (ET-1) has been observed in this model, thus we decided to study the relaxation induced by ET-1 on the aorta. Non-pregnant or pregnant Wistar rats (n = 7 by group) were fed for 7 days (day 13-day 20) on a nitroarginine-enriched diet (L-NNA, 0.063% i.e. 30 mg/kg/day) or a control diet. Systolic blood pressure, measured by the tail cuff method on conscious rats at day 20 of gestation, was raised by the chronic L-NNA treatment (mean +/- s.e.m., mmHg, p < 0.001: pregnant L-NNA treated, 145 +/- 1.84 vs. pregnant control, 101 +/- 2.00 and non-pregnant L-NNA treated, 148 +/- 3.11 vs. non-pregnant control, 119 +/- 1.80). On day 20 ex vivo aortic ring relaxation was produced by ET-1 in vessels previously precontracted with norepinephrine only when endothelium was present. In control rats, ET-1 (10(-8) to 5 x 10(-8) M) produced a short but significant relaxation (mean value between 4 to 19%) followed by a long-lasting contracting phase, and a higher ET-1 concentration (10(-7) M) only produced contraction. Chronic L-NNA treatment decreased the level of relaxation (at least p < 0.05, in non-pregnant and pregnant rats) and with a 30 min L-NAME (10(-4) M) preincubation, relaxation was completely inhibited in non-pregnant and pregnant rats. BQ-123, an ETA receptor antagonist, did not produce any effect on ET-1 induced relaxation. BQ-788, an ETB receptor antagonist, significantly decreased it. In conclusion, in female rats, as in male rats, ET-1 induces a transient relaxation in the preconstricted aorta which involves endothelial ETB receptors. Despite a decrease in the systemic vascular reactivity during late gestation, the vasodilating and vasoconstricting properties of ET-1 on the aorta are not changed.

Animals↗

PubMed1998

[Nitric oxide and isolated aortic contraction in a pregnant hypertension model by the inhibition of nitric oxide synthase in pregnant Wistar rats].

During gestation endothelium induces decreases in vascular responses to vasopressor agents but endothelium disease is followed by hypertension and enhanced vascular reactivity during preeclampsia. In a rat model of preeclampsia induced by NO synthase inhibition we study here isolated aortic contractions. From day 13 of gestation 2 groups of Wistar female rats were fed control (C) or nitro-arginine enriched diets (0.063%, i.e. 30 mg/kg/d) (treated) (T). On gestational day 20 systolic blood pressure (SBP, mmHg) is measured by tail cuff method and isolated thoracic ring aorta contractions are studied after depolarisation (KCl 60 mM) or norepinephrine (cumulative concentrations 10-9 M-10-5 M). After chronic NOS inhibition, hypertension develops: SBP is 154 +/- 2.17 in T and 116 +/- 3.75 in C, p < 0.01 and significant proteinuria (mg/d) appears: T, 63.4 +/- 21.6 versus C 3.08 +/- 0.48, p < 0.01. NO synthase inhibition in treated rats impairs the depressed contractile response obtained in the presence of endothelium in control rats but addition of L-arginine suppresses the effect of nitroarginine. Taking in account our results and those described in literature it appears that L-arginine treatment could ameliorate some pathologic pregnancies.

Animals↗

PubMed1998

[Hypotensive effect of endothelin-1 in a rat model of pre-eclampsia].

Hypertensive pregnant rats with inhibition of NO synthase are frequently considered as model of pre-eclampsia with proteinuria, hypertension and elevated endothelin (ET-1) blood levels. We describe here the cardiovascular in vivo effects of ET-1 in this rat model since ET-1 and NO are both important vasoactive mediators in uteroplacental circulation. From day 13 of gestation 2 groups of Wistar female rats were fed control (C) or nitroarginine enriched diet (0.063%, Treated: T). On gestational day 20 mean arterial pressure (MAP, mmHg) was measured via a carotid catheter in pentobarbital (60 mg/kg) anesthetized rats. After chronic NO synthase inhibition hypertension develops; MAP on day 20: 158 +/- 2.2 in T and 113 +/- 2.2 in C, p < 0.001. ET-1 bolus injection (0.1 nmol/kg) is rapidly followed by a decrease in blood pressure significantly more important in T: -46 +/- 5.1 than in C: -30 +/- 2.2. In vivo depressor effect is blocked by the specific antagonist BQ-788. After inhibition of cycloxygenase with acetylsalicylic acid (27 mumol/kg, 30 min before) the hypotension is not modified. Since NO and PGI2 productions are not expected in our conditions, vasodepressor effect can be explained by an endothelial hyperpolarazing factor (EDHF). In conclusion in vivo ET-1 hypotensive effects in pregnant rats are mediated by ETB receptors and more pronounced in hypertensive NO-deprived animals.

Animals↗

PubMed1995

Endogenous nitric oxide is not involved in acute parathyroid hormone-induced hypotension in rat: effect of hypertension and hypoparathyroid status.

The present study investigated the acute hypotensive effect of parathyroid hormone (PTH) in anesthetized adult spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto rats. Furthermore, in order to determine the possible contribution of nitric oxide (NO), a mediator of endothelium-dependent vasorelaxation, hypotensive responses to PTH were obtained in the presence of NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthesis. The hypotensive effect of PTH (expressed as % of baseline blood pressure) was similar for the two strains. In the presence of L-NAME (18.5 mumol/kg), both strains demonstrated a similar hypotensive response to PTH, indicating that the hypotensive response to PTH is NO-independent.

Animals↗

PubMed1995

[Chronic and acute effect of cycletanine in NO-dependent hypertensive pregnant rats].

Decreased response to vasopressor agents characterizes pregnancy. Endothelium-derived relaxing factors and vasodilating prostaglandins play an important role in the vascular tone during pregnancy. Since inhibition of nitric oxide (NO) biosynthesis induced by NO2-arginine enriched diet produced hypertension we measured in vivo cardiovascular responses to PGF2 alpha, L-arginine (L-arg) and cicletanine (Cic, IPSEN, France) which enhances PGI2 production. From day 13 to day 20 of gestation 4 groups of female Wistar rats were fed NO2-arg (31 mg/kg/d), NO2-arg+Cic (10 mg/kg/d), Cic enriched or control diet (C). Mean arterial pressure (MAP) was measured via a carotid catheter in anesthetized rats. Injection of PGF2 alpha (50 micrograms/kg) in jugular vein significantly increased MAP in the NO2-arg group versus, NO2-arg+Cic, Cic and C group (+23.5 +/- 3.3 vs +15.7 +/- 2.2, +15.8 +/- 2.2 and +17 +/- 1.85 mmHg; p < 0.01). Injection of L-arg (100 mg/kg) or Cic (1 mg/kg) 5 min before PGF2 alpha produced no modification in MAP in C and Cic group. Likewise in NO2-arg group injection of L-arg or Cic produced a diminished pressor response to PGF2 alpha (+23.5 +/- 3.3 vs -17.5 +/- 1.7 mmHg; p < 0.05 and +15.2 +/- 2.4 mmHg; p < 0.01 respectively). In NO2-arg+Cic group, only injection of Cic induced a diminished pressor response to PGF2 alpha which is more important without L-arg (+15.7 +/- 2.2 vs +9.1 +/- 1.3 mmHg; p < 0.001) or with L-arg (+13.6 +/- 1.5 vs +9.1 +/- 1.3 mmHg; p < 0.01). Cicletanine also significantly diminished the proteinuria in the NO2-arg+Cic group versus NO2-arg group (13.9 +/- 4.36 vs 63.4 +/- 21.6 mmHg; p < 0.01). IN CONCLUSION, chronic NO synthesis inhibition enhanced blood pressure and pressor responses to PGF2 alpha during pregnancy in rats. Chronic administration of cicletanine in Wistar pregnant rats decreases the response to vasopressor agents like PGF2 alpha. Moreover acute and chronic administration of cicletanine blunted the pressor effect, which was lower than in normal gestation.

Animals↗

PubMed1995

Blood pressure effects of calcium intake in experimental models of hypertension.

Calcium intake has been implicated as being an important factor in the development and treatment of hypertension. The mechanisms underlying the relationship between calcium and blood pressure are not yet clearly defined. Experimental studies have documented an inverse association between calcium intake and blood pressure level. For 15 years it has been shown that calcium supplementation is effective in lowering blood pressure in hypertensive rats and, on the other hand, calcium deprivation results in increased blood pressure levels. Enriched calcium diets decrease blood pressure in genetic hypertension displayed by spontaneously hypertensive rats (SHR), stroke-prone SHR, Lyon hypertensive rats or Dahl salt-sensitive rats and, in volume-dependent hypertension induced by saline and mineralocorticoid or angiotensin II administration in Wistar or Sprague-Dawley rats. Efficacy is observed with calcium carbonate added in the diet and with calcium chloride or calcium gluconate in drinking water. Compared with the normal level in the diet (0.5% to 1%), calcium supplementation represents mainly a fourfold increase whose effect is more intense in young weaning animals treated for a long-lasting period (4 to 10 weeks).

Animals↗

PubMed1994

Characterization of endothelium-derived relaxing factor involvement in the potentiating effect of parathyroidectomy on norepinephrine-induced rat aortic contraction.

Previous results have shown that the contractile response to norepinephrine (NE) was enhanced in isolated aortae from SHR and normotensive Wistar parathyroidectomized rats. In this work we sought to characterize the contribution of endothelium-derived relaxing factor (EDRF) release to this effect which is not linked to hypertension. Parathyroidectomy (PTX) was performed by surgery on 5 week-old male Wistar rats. Five weeks later intact (E+) and rubbed (E-) aortic rings were mounted in an organ chamber for isometric tension recording. KCl-induced contractions were potentiated in PTX E+ aortae compared to sham operated (SO), (P < 0.05), but not in denuded E- aortae. Similarly NE (1 nM- 10 microM) induced a potentiated contractile response in PTX E+ (P < 0.01), but not in PTX E- rings; nevertheless the sensitivity did not change. After removal of endothelium, the expected enhanced contraction and sensitivity observed in SO rats was not present in PTX. The NO synthase inhibitor L-NAME (20 microM), enhanced sensitivity to NE in SO but not in PTX E+ aortic rings. In addition, hemoglobin (Hb, 10 microM) enhanced NE contraction in SO (P < 0.01) aortic rings, but to a lesser extent in PTX rat aortae. Moreover, in the presence of L-NAME or Hb, SO and PTX aortae displayed a similar contraction. Superoxide dismutase (SOD, 150 U/ml) diminished the NE contraction since NO was protected from degradation but the difference was still present between SO and PTX rat aortae, ruling out the possible implication of superoxide anions in the hyperreactivity of PTX aortae. On the other hand, A23187, which induces EDRF release, reduced the level of NE contraction as expected, but suppressed the PTX enhancing effect and in calcium-free solution the enhancement of contraction after PTX was not observed. These experiments extend to the rat the observations previously obtained in rabbit aorta: extracellular calcium is a major determining factor in NO production. Acetylcholine and A23187 (cumulative doses) produced an endothelium-dependent relaxation which was not significantly modified in NE-pre-contracted PTX aortae compared to SO aortae. L-arginine (100 microM), reversed the L-NAME inhibitory effect and induced an attenuated endothelium-dependent relaxation in PTX vessels (P < 0.01). In conclusion, in rat isolated aortae the enhancing effect of parathyroidectomy on norepinephrine and KCl contractions is due to a diminished endothelial nitric oxide production. This might arise via a decrease of the constitutive NO synthase activity in an extracellular calcium-dependent manner.

Acetylcholine↗

PubMed1994

Pharmacokinetics of the enantiomers of tertatolol in the rat after oral and intravenous administration.

1. Plasma concentrations of the two enantiomers of tertatolol were determined by gc/ms. Deuterium labelling of one of the tertatolol enantiomers was used for chiral discrimination. 2. No isotope effects were observed following simultaneous oral administration of tertatolol and [2H9]tertatolol. 3. After intravenous administration of the pseudoracemate or of each enantiomer separately, (+)-tertatolol showed a lower total clearance and volume of distribution, compared to the (-) enantiomer. 4. After oral administration of the pseudoracemate or of each enantiomer separately, no substantial difference in bioavailability were observed between the enantiomers.

Administration, Oral↗

PubMed1994

Parathyroid cross-transplantation and development of high blood pressure in rats.

To clarify further the relationships between parathyroid glands and the development of hypertension, we studied the effect of cross-transplantation of these glands from young hypertensive rats in normotensive recipients. The parathyroid glands were isolated in 5-week-old hypertensive rats of the Lyon (male and female) and Milan (only male) strains and immediately grafted into the corresponding, just parathyroidectomized normotensive rats of the same age. Control rats were either sham-operated or grafted with the glands of the same normotensive strain. Plasma calcium concentration immediately decreased after parathyroidectomy (PTX) and returned to near normal values 3 weeks after the graft. Systolic blood pressure increased slightly, but significantly, in normotensive animals grafted with hypertensive glands compared with that in normotensive control rats (mean increase, +9 mm Hg in males; +5 mm Hg in females). In conclusion, parathyroid gland transplantation from the hypertensive strain is able to chronically enhance blood pressure in the normotensive animal. The parathyroid hypertensive factor recently described may be implicated in these two hypertensive strains. Our data extend observations obtained previously in SHRs and stroke-prone SHRs and add further evidence for a major function of parathyroid glands in experimental hypertension.

Animals↗

PubMed1994

Ions, parathyroids, and genetic hypertension.

Several reports suggested an involvement of parathyroid function in blood pressure regulation in animals and humans: hyperparathyroid subjects frequently display an elevated systolic blood pressure and young mild hypertensive patients show enhanced serum PTH levels. Moreover, removal of parathyroid glands (PTX) in young rats attenuates and delays the development of mineralocorticoid and genetic hypertension. In addition, in vivo cardiovascular reactivity to norepinephrine in PTX rats from both spontaneously the hypertensive rat (SHR) and Lyon hypertensive rat (LH) strains is decreased, as is calcium content in aortic and heart fragments. Moreover, parathyroid grafts from SHR, stroke-prone SHR (SHR-SP), LH, or Milan hypertensive rats (MHS) into previously parathyroidectomized normotensive recipient rats have been shown to induce an increase in blood pressure. Recently, in essential hypertensive patients and in SHR, a circulating hypertensive factor has also been described. Produced by the PTX in SHR, this factor is inversely related to the amount of dietary calcium. It appears, therefore, that the PTX plays a major role in experimental and probably also in human hypertension.

Animals↗

PubMed1993

Age, endothelium and aortic reactivity to calcium in Wistar rat.

The influence of age from (9 to 72 weeks) was investigated on contractions elicited by calcium in Wistar rat aortic rings with and without endothelium. The arteries were either depolarized by KCl or exposed to Bay K 8644 and concentration-effect curves to cumulative additions of CaCl2 were constructed. Whether the endothelium was present or not, the potency of CaCl2 but not its maximal effect decreased with age. The same decrease in potency was obtained with Bay K 8644, in the presence of which the maximal contractions were increased at 72 weeks. In K+ depolarized arteries, nitrendipine (10(-10) and 10(-9) M) markedly decreased maximal contraction elicited by CaCl2 and it moderately displaced to the right the concentration-effect curves. The endothelium did not modify the responses to CaCl2 of depolarized arteries, in the absence of nitrendipine. However it markedly enhanced the depressor effect of nitrendipine in these preparations, and it impaired contractions elicited by calcium in the presence of Bay K 8644. These effects of the endothelium were both less at 72 weeks than at younger ages. These experiments show a possible impairment of the inhibitory effect of the endothelium in 72 week old rats in the presence of both agonist and antagonist dihydropyridines.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1993

Endothelium-derived relaxing factor, hypertension and chronic parathyroidectomy in spontaneously hypertensive and Wistar-Kyoto rats.

1. Parathyroidectomy (PTX) lessens the development of hypertension in young spontaneously hypertensive rats (SHR) and the involved mechanisms remain to be elucidated. We have studied here the aortic vascular reactivity to both norepinephrine (NE) and acetylcholine in 10 week old male PTX SHR and Wistar-Kyoto (WKY) rats. 2. Depolarized (KCl 100 mmol/L) and NE (1 mumol/L or cumulative 10(-9)-10(-5) mol/L) precontracted intact aortic rings from PTX rats show a significant and unexpected increase of maximal contractile responses in normotensive and hypertensive animals. These results are also obtained with low extracellular ionized calcium levels (0.625 and 0.9 mmol/L) similar to PTX ionized plasma calcium. N omega-Nitro-L-arginine methyl ester (L-NAME, 20 mumol/L) potentiates the NE response in SHR and WKY rats, more significantly in control than in PTX animals. 3. In the presence of indomethacin (10 mumol/L) in SHR the potentiating effect of PTX on NE contraction is still observed, ruling out a specific production of vasoconstrictors from the arachidonic cascade by the PTX rat aortic endothelium. 4. After PTX a moderate impairment of acetylcholine relaxant responses is observed in SHR and WKY rat aortas and basal aortic cyclic guanosine 3'-5' monophosphate (cGMP) content is also decreased; nevertheless sodium nitroprusside causes a similar relaxation. Furthermore in L-NAME-treated aortas and in the presence of L-arginine (100 mumol/L), acetylcholine (1 mumol/L) produces a significantly less pronounced relaxation in PTX rats. 5. In conclusion, the enhancement of NE contractile response in PTX rat aortas is not linked to the strain but probably related to a decrease in endothelial nitric oxide (NO) release or activity. Enhancement of force generation that we describe does not directly participate in the attenuated hypertension observed in SHR after parathyroidectomy.

Acetylcholine↗

PubMed1993

[Genetic hypertension in the rat is partially dependent of parathyroid glands. Results of a crossed transplantation trial].

The parathyroid hypertensive factor (PHF) is present in the plasma of SHR rats. The authors of this study set out to determine whether this factor was also present in the Lyon (LH male and female) and Milan (MHS male) hypertensive rats. Five week old normotensive rats (LN and MNS) were transplanted with the parathyroid glands of LH and MHS rats immediately after parathyroidectomy (PTX). Plasma calcium fell rapidly after PTX but returned to physiological levels, confirming the functional activity of the graft. Systolic blood pressures of transplanted rats were significantly higher than normotensive LN and MNS controls. These results confirm the role of the parathyroid glands in the genesis of hypertension in Lyon and Milan male and female rats. They suggest that PHF may be implicated in the hypertensive mechanisms of these two models of genetic hypertension.

Animals↗

PubMed1991

Effect of parathyroidectomy on development of hypertension and atrial responsiveness in spontaneous hypertensive rats.

1. In order to further clarify the relationships between parathyroid function and development of hypertension, the effects of parathyroidectomy (PTX) on blood pressure and on responsiveness of atria isolated from spontaneous hypertensive rats (SHR) were examined. 2. PTX was carried out in 6-week-old SHR and normotensive Wistar rats. The experiments were performed 2 weeks after surgery. 3. PTX reduced the plasma calcium concentration and decreased atrial calcium content in SHR. On the other hand, basal contractile force and beat frequency of isolated atria were higher in PTX SHR than in sham-operated SHR. In response to cumulative addition of isoprenaline, atria from PTX SHR displayed diminished inotropic and chronotropic responses compared with sham-operated SHR. Similar results were obtained in atria isolated from Wistar rats. When calcium sensitivity was studied in atria from Wistar rats, basal and isoprenaline-induced maximum contractile forces were higher in PTX group than in the sham-operated group. Nevertheless, basal and isoprenaline-induced maximum contractile forces, determined at the respective plasma ionized calcium concentration of PTX and sham-operated groups (0.83 and 1.22 mmol/L), were not significantly different. 4. Our results do not favour a role for alteration in atrial activity as a causal mechanism in delayed development of experimental genetic hypertension after parathyroidectomy.

Animals↗