Effect of NG-monomethyl-L-arginine on arcade arterioles of rat spinotrapezius muscles

1991 ◽  
Vol 261 (1) ◽  
pp. H46-H52 ◽  
Author(s):  
T. Nakamura ◽  
R. L. Prewitt
Keyword(s):  
Specific Inhibitor ◽  
Onset Of Action ◽  
Adrenoceptor Antagonist ◽  
No Formation ◽  
Vasoactive Substances ◽  
Adrenoceptor Agonist ◽  
Before And After ◽  
Arteriolar Tone ◽  
Arteriolar Diameter

The effect of the specific inhibitor of nitric oxide (NO) formation NG-monomethyl-L-arginine (L-NMMA) on resting arteriolar diameter and on actions of both endothelium-dependent and -independent vasoactive substances was investigated using intravital microscopy in rats. The spinotrapezius muscle of anaesthetized normotensive rats was suspended in a Krebs-Henseleit bath containing tetrodotoxin (3 x 10(-7) M), indomethacin (2.8 x 10(-5) M), and propranolol (10(-6) M) to block sympathetic nerve conduction, prostacyclin formation, and beta-adrenergic receptors, respectively. Acetylcholine (ACh), nitroprusside (NP), norepinephrine (NE), phenylephrine (PE), and guanabenz (GB) were topically applied before and after superfusion of L-NMMA (10(-5) to 10(-4) M). Superfusion of L-NMMA reduced arteriolar diameter and caused dose-dependent increases in arteriolar tone. The onset of action of L-NMMA was nearly immediate. L-NMMA inhibited vasodilator responses to the endothelium-dependent vasodilator ACh but not to the endothelium-independent NP. NE induced dose-related vasoconstriction that was significantly potentiated by L-NMMA. These effects were partially reversed by addition of L-arginine (10(-3) M). Potentiation of vasoconstriction elicited by NE was still observed after inhibition of alpha 1-adrenoceptors with prazosin, but potentiation was abolished by the alpha 2-adrenoceptor antagonist yohimbine. L-NMMA potentiated arteriolar vasoconstriction elicited by the alpha 2-adrenergic receptor agonist GB but not by the alpha 1-adrenoceptor agonist PE. These findings with L-NMMA suggest that resting diameter of arterioles is modulated by endogenous NO biosynthesis and that endothelium-dependent vasodilators act through the formation of endogenous NO to exert their action in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of α-adrenoceptor agonists and antagonists on thyroid hormone secretion

1985 ◽  
Vol 108 (2) ◽  
pp. 184-191 ◽  
Author(s):  
Bo Ahrén
Keyword(s):  
Thyroid Hormone ◽  
Dose Level ◽  
Hormone Secretion ◽  
High Dose ◽  
Inhibitory Effects ◽  
High Dose Level ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists

Abstract. The effects of various α-adrenoceptor agonists and antagonists on blood radioiodine levels were studied in mice pre-treated with 125I and thyroxine. The non-selective α-adrenoceptor agonist noradrenaline and the selective α1-adrenoceptor agonist phenylephrine both enhanced blood radioiodine levels. Noradrenaline was more potent than phenylephrine. Contrary, the selective α2-adrenoceptor agonist clonidine depressed basal levels of blood radioiodine. The non-selective α-adrenoceptor antagonist phentolamine and the selective α1-adrenoceptor antagonist prazosin both inhibited the noradrenaline-induced elevation of radioiodine levels, whereas the α2-adrenoceptor antagonist yohimbine had no such effect, except at a high dose level. All three α-adrenoceptor agonists, noradrenaline, phenylephrine and clonidine, inhibited the radioiodine response to TSH. In addition, TSH-induced increase in radioiodine levels was inhibited by prazosin, whereas yohimbine had no effect. Phentolamine inhibited the radioiodine response to TSH when given 2 h prior to TSH, whereas when given 15 min prior to TSH the response to TSH was potentiated by Phentolamine. It is concluded, that under in vivo conditions in the mouse, α1-adrenoceptor activation stimulates basal thyroid hormone secretion and inhibits TSH-induced thyroid hormone secretion. Further, α2-adrenoceptor activation inhibits basal thyroid hormone secretion. In addition, TSH-induced thyroid hormone secretion is inhibited by α1-adrenoceptor antagonism. Thus, α-adrenoceptors induce both stimulatory and inhibitory effects of thyroid function.

scholarly journals Differential in vivo Sensitivity of Melanophores and Xanthophores to Catecholamines in Winter Flounder (Pseudopleuronectes Americanus Walbaum) Integumentary Patterns

1985 ◽  
Vol 114 (1) ◽  
pp. 649-659
Author(s):  
D. Burton
Keyword(s):  
Winter Flounder ◽  
Pseudopleuronectes Americanus ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Albedo Change ◽  
Differential Responses

The catecholamines, adrenalin, dopamine and noradrenalin induce differential aggregation of melanophores in black-adapted winter flounder, Pseudopleuronectes americanus, paralleling patterning responses to albedo change. These differential responses to catecholamines suggest that the patterning mechanism in this species is largely dependent on a balance between neural aggregating and dispersing elements. The α-adrenoceptor agonist phenylephrine evokes paling in all pattern components in blackadapted flounder, whilst the α-adrenoceptor antagonist phentolamine darkens white-adapted flounders. The α-adrenoceptor agonist isoproterenol and the α-adrenoceptor antagonist propranalol have no effect on chromatophores of white-adapted flounder, but induce pallor in blackadapted flounder, which is interpreted as non specific. Noradrenalin elicits patterning responses in chromatically decentralized flounder, although the duration of pallor is shorter. The xanthophores, which are dispersed by a pituitary factor, will aggregate in response to high catecholamine doses.

Microvascular response to blockade of prostaglandin synthesis in rat skeletal muscle

1982 ◽  
Vol 243 (1) ◽  
pp. H51-H60 ◽  
Author(s):  
J. E. Faber ◽  
P. D. Harris ◽  
I. G. Joshua
Keyword(s):  
Skeletal Muscle ◽  
Cremaster Muscle ◽  
Local Blood Flow ◽  
Local Inhibition ◽  
Microvascular Response ◽  
Before And After ◽  
Endogenous Prostaglandins ◽  
The Moment ◽  
Arteriolar Tone ◽  
Arteriolar Diameter

The contribution of endogenous prostaglandins (PGs) to the control of arteriolar diameter in the microcirculation is incompletely defied and has only been studied in drug-anesthetized animals. To test the possibility that endogenous PGs are tonically released to exert a net dilator influence at certain levels in the microcirculation, television microscopy was used to quantitate the arteriolar responses in the rat cremaster muscle to local blockade of PG synthesis with indomethacin. Rats were decerebrated by a midcollicular transection and were allowed to recover from surgical anesthesia. The cremaster muscle with intact circulation and innervation was suspended by sutures in a temperature-controlled Krebs bath. Diameters, vasomotion frequency, and vasomotion amplitude of arterioles at several anatomic levels were measured before and after local inhibition of PG synthesis in the presence and absence of alpha-adrenergic receptor blockade. Inhibition of PG synthesis produced marked constriction (42-66% of control) at all arteriolar levels, with greater responses occurring in the smaller arterioles. PG synthesis blockade increased vasomotion frequency in arterioles that exhibited spontaneous vasomotion during control periods, and blockade induced vasomotion in vessels lacking spontaneous vasomotion. Pretreatment with phentolamine significantly attenuated the constriction and augmentation of vasomotion. These data indicate that dilator PGs participate in the moment-to-moment regulation of arteriolar tone and local blood flow in skeletal muscle. Further, their mechanism of action may involve alterations in neuronal norepinephrine release or alpha-receptor sensitivity.

Regulation of arteriolar tone and responses via L-arginine pathway in skeletal muscle

1992 ◽  
Vol 262 (4) ◽  
pp. H987-H992 ◽  
Author(s):  
G. Kaley ◽  
A. Koller ◽  
J. M. Rodenburg ◽  
E. J. Messina ◽  
M. S. Wolin
Keyword(s):  
Skeletal Muscle ◽  
Vascular Tone ◽  
Topical Administration ◽  
Systemic Blood Pressure ◽  
Vasoactive Agents ◽  
Skeletal Muscle Microcirculation ◽  
Arteriolar Tone ◽  
Dose Dependent ◽  
Arteriolar Diameter

With in vivo television microscopy, changes in arteriolar diameter to topical administration of various vasoactive agents were examined in the absence or in the presence of NG-monomethyl-L-arginine (L-NMMA, topical 100 microM) or NG-nitro-L-arginine (L-NNA, 2.5 microM, 20 microliters/min ia), specific inhibitors of endothelium-derived relaxing factor (EDRF) biosynthesis. In cremaster muscle arterioles (15-22 microns) of rats (n = 6-11), dilations to acetylcholine (1-100 ng) were significantly inhibited (60-70%) by either of the arginine analogues. This inhibition was reversed by subsequent administration of 1 mM L-arginine. Dose-dependent constriction to norepinephrine was enhanced by L-NMMA. Indomethacin treatment reduced arteriolar dilation to bradykinin (BK, 1-100 ng), which was significantly inhibited by additional administration of L-NNA. Application of L-NNA first, followed by additional indomethacin, elicited similar results. Dilations to sodium nitroprusside and adenosine were not reduced in the presence of the inhibitors. L-NMMA or L-NNA caused no change in systemic blood pressure but elicited a significant reduction in arteriolar diameter; this effect was not reversed by 1 mM L-arginine. These data demonstrate the presence of an L-arginine pathway to produce EDRF (nitric oxide) in skeletal muscle microcirculation that mediates and/or modulates arteriolar responses to vasoactive agents and could contribute to the regulation of basal vascular tone.

Evoked secretion of [3H]noradrenaline and ATP from nerve varicosities isolated from the myenteric plexus of the guinea pig ileum

1988 ◽  
Vol 66 (3) ◽  
pp. 369-375 ◽  
Author(s):  
James R. Hammond ◽  
Wenda F. MacDonald ◽  
Thomas D. White
Keyword(s):  
Guinea Pig ◽  
Myenteric Plexus ◽  
Longitudinal Muscle ◽  
Secretory Vesicles ◽  
Effective Inhibitor ◽  
Guinea Pig Ileum ◽  
Release Of Noradrenaline ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist

Neuronal varicosities, isolated from the myenteric plexus of guinea pig ileum longitudinal muscle, were incubated with [3H]noradrenaline to label the contents of the noradrenergic secretory vesicles. Exposure of these varicosities to KCl, nicotine, or acetylcholine resulted in the Ca2+-dependent release of [3H]noradrenaline. Veratridine also evoked a large efflux of [3H] from this preparation, but this release was only partially Ca2+ dependent. The α2-adrenoceptor agonist, clonidine, inhibited the K+-, nicotine-, and acetylcholine-induced release of [3H]noradrenaline. Similarly, exogenously administered (−)noradrenaline was an effective inhibitor of the K+-evoked release of [3H]noradrenaline. The α2-adrenoceptor antagonist, yohimbine, antagonized the inhibitory actions of both clonidine and (−)noradrenaline on the K+-evoked release of [3H]noradrenaline from myenteric varicosities. Nicotine, acetylcholine, KCl, and veratridine also released ATP from these guinea pig ileal myenteric varicosities. However, the evoked release of ATP was unaffected by clonidine. These results indicate that myenteric varicosities can take up and release [3H]noradrenaline and that they possess presynaptic α2-adrenoceptors which, when activated, inhibit the release of [3H]noradrenaline. These receptors may play a role in modulating the release of noradrenaline in the myenteric plexus in vivo. In addition, the present results suggest that ATP and [3H]noradrenaline may not be released from the same population of secretory vesicles in neuronal varicosities isolated from guinea pig ileum longitudinal muscle.

Potentiation of Bradykinin by Angiotensin-(1-7) on Resistance Vessels of Hypertensive Rats, Studied in Vivo .

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 696-696
Author(s):  
Liliam Fernandes ◽  
Zuleica B Fortes ◽  
Dorothy Nigro ◽  
Regina Scivoletto ◽  
Robson A S Santos ◽  
...  
Keyword(s):  
Topical Application ◽  
Ace Inhibition ◽  
Pharmacological Effects ◽  
Hypertensive Rats ◽  
Specific Receptor ◽  
Resistance Vessels ◽  
Before And After ◽  
Arteriolar Diameter

P19 Objective: To verify the Angiotensin-(1-7) [Ang-(1-7)]-activity on Bradykinin (BK)-induced vasodilation in SHR mesenteric arterioles, in vivo-in situ. Methods: Arteriolar diameter was measured by intravital microscopy before and after topical application of BK(1pmol), Acetylcholine(ACh 1.6nmol), Sodium nitroprusside (SNP 38pmol) or Histamine (5.4nmol) in the absence or presence of Ang-(1-7) (100pmol). To investigate the Ang-(1-7)/BK interaction, treatments were employed through topical application of antagonists of BK (HOE140,100pmol), Ang-(1-7)(A779,100pmol)and potassium channel (tetraethylammoniun - TEA,90pmol), with an inhibitor of NOSynthase (L-NAME 10nmol) and after cyclooxygenase blockade (indomethacin 5mg/Kg or diclofenac 2.5mg/Kg). To evaluate the effect of ACE- and/or AT 1 blockade on Ang-(1-7)/BK interaction, rats were treated for 21 days with enalapril, quinapril (10mg/Kg), losartan (15mg/Kg) or enalapril + losartan (10 and 15 mg/Kg, respectively). In those enalapril-treated rats the effect of BK (1pmol) was also analysed in the presence of A779 (100pmol). Results: BK-induced vasodilation, but not ACh, SNP or Histamine responses, was increased in the presence of Ang-(1-7) (4.96±0.7% vs 9.07±1.0% * ).This interaction was abolished by HOE (1.11±0.8% * ), A779 (5.13±0.6% * ), TEA (3.37±0.5% * ), indomethacin (1.73±0.4% * )and diclofenac (3.63±0.5% * ), whereas L-NAME did not modify the Ang-(1-7)-potentiating activity. The BK-potentiation by Ang-(1-7) was also observed after enalapril (10.57±0.5% * ), quinapril (8.9±0.7% * ), losartan (9.93±1.2% * ) and enalapril + losartan (10.59±0.5% * ). Enalapril increased the BK-vasodilation(8.21±0.7% * ), but this effect was reversed in the presence of A779 (4.27±0.5% * ). * p≤0.05 Conclusion: In the SHR microcirculation Ang-(1-7) potentiates BK through a specific receptor, probably releasing prostaglandins and EDHF. Our results indicate that the BK-potentiation by Ang-(1-7) may occur endogenously and contribute to the pharmacological effects of ACE inhibition. HOE 140 and Quinapril were gifts from HOECHST and Warner Lambert, respectively.

Role of L-arginine-derived nitric oxide in cholinergic dilation of gastric arterioles

1993 ◽  
Vol 265 (6) ◽  
pp. H2110-H2116
Author(s):  
R. Y. Chen ◽  
G. Ross ◽  
K. Y. Chyu ◽  
P. H. Guth
Keyword(s):  
Nitric Oxide ◽  
Vascular Tone ◽  
Topical Administration ◽  
Microscopy Technique ◽  
No Formation ◽  
Resistance Vessels ◽  
Gastric Circulation ◽  
Arteriolar Diameter

The role of L-arginine-derived nitric oxide (NO) in cholinergic vasodilation of resistance vessels was studied in the intact stomach of the rat, utilizing an in vivo microscopy technique. Two L-arginine analogues, NG-monomethyl-L-arginine (L-NMMA) and nitro-L-arginine methyl ester (L-NAME), were used to block NO synthesis. Cholinergic dilation of gastric submucosal arterioles was induced by topical application of various concentrations of acetylcholine (ACh) (10(-7)-10(-4) M). Intravenous but not topical administration of L-NMMA and L-NAME caused an increase in arterial pressure. Intravenous or topical L-NAME reduces resting arteriolar diameter. These findings support the contention that NO formation modulates basal vascular tone and suggest that NO release may play a significant role in the regulation of the gastric circulation. L-Arginine analogues attenuated the arteriolar dilating effect of ACh but not adenosine or nitroglycerin. Substantial arteriolar responses to ACh remained after systemic or topical treatment with either L-NMMA or L-NAME. These results indicate that the L-arginine-NO pathway accounts only in part for ACh-induced vasodilation in gastric resistance vessels in vivo.

ATP-mediated release of arachidonic acid metabolites from venular endothelium causes arteriolar dilation

2001 ◽  
Vol 280 (6) ◽  
pp. H2616-H2622 ◽  
Author(s):  
Leah W. Hammer ◽  
Alison L. Ligon ◽  
Robert L. Hester
Keyword(s):  
Air Bubbles ◽  
Cremaster Muscle ◽  
In Vivo Microscopy ◽  
Relaxing Factor ◽  
Acid Metabolites ◽  
Male Golden Hamsters ◽  
Arteriolar Tone ◽  
Arteriolar Diameter ◽  
Venular Endothelium

This study was designed to test the hypothesis that venular administration of ATP resulted in endothelium-dependent dilation of adjacent arterioles through a mechanism involving cyclooxygenase products. Forty-three male golden hamsters were anesthetized with pentobarbital sodium (60 mg/kg ip), and the cremaster muscle was prepared for in vivo microscopy. ATP (100 μM) injected into venules dilated adjacent arterioles from a mean diameter of 51 ± 4 to 76 ± 6 μm ( P < 0.05, n = 6). To remove the source of endothelial-derived relaxing factors, the venules were then perfused with air bubbles to disrupt the endothelium. Resting arteriolar diameter was not altered after disruption of the venular endothelium (51 ± 5 μm), and the responses to venular ATP infusions were significantly attenuated (59 ± 4 μm, P < 0.05). To determine whether the relaxing factor was a cyclooxygenase product, ATP infusion studies were repeated in the absence and presence of indomethacin (28 μM). Under control conditions, ATP (100 μM) infusion into the venule caused an increase in mean arteriolar diameter from 55 ± 4 to 78 ± 3 μm ( P < 0.05, n = 6). In the presence of indomethacin, mean resting arteriolar tone was not significantly altered (49 ± 4 μm), and the response to ATP was significantly attenuated (54 ± 4 μm, P < 0.05, n = 6). These studies show that increases in venular ATP concentrations stimulate the release of cyclooxygenase products, possibly from the venular endothelium, to vasodilate the adjacent arteriole.

Peptidases modulate bradykinin-induced arteriolar dilation in the hamster cheek pouch

1994 ◽  
Vol 266 (1) ◽  
pp. H93-H98 ◽  
Author(s):  
X. P. Gao ◽  
P. Anding ◽  
R. A. Robbins ◽  
S. I. Rennard ◽  
I. Rubinstein
Keyword(s):  
Proteinase Inhibitors ◽  
Neutral Endopeptidase ◽  
Cheek Pouch ◽  
Induced Responses ◽  
Hamster Cheek Pouch ◽  
Before And After ◽  
Peripheral Microcirculation ◽  
Membrane Bound ◽  
Arteriolar Diameter

The purpose of this study was to investigate whether angiotensin-converting enzyme (ACE; EC 3.4.15.1) and neutral endopeptidase (NEP; EC 3.4.24.11), two membrane-bound metalloenzymes that are widely distributed in the peripheral microcirculation and degrade kinins very effectively, modulate bradykinin-induced arteriolar dilation in vivo. Using intravital microscopy, we measured diameter of second-order arterioles in the hamster cheek pouch during suffusion of bradykinin (0.1–10.0 microM) before and after topical application of captopril (10.0 microM) and phosphoramidon (10.0 nM). We found that each inhibitor significantly potentiated bradykinin-induced increase in arteriolar diameter (P < 0.05). Suffusion of other proteinase inhibitors (excluding ACE and NEP inhibitors) had no significant effect on bradykinin-induced responses. Captopril and phosphoramidon did not potentiate isoproterenol (0.1 microM)-induced arteriolar dilation in the cheek pouch. Collectively, these data indicate that ACE and NEP each plays an important role in regulating bradykinin-induced vasorelaxation in the peripheral microcirculation in vivo.

L-arginine analogues blunt prostaglandin-related dilation of arterioles

1993 ◽  
Vol 264 (4) ◽  
pp. H1194-H1199 ◽  
Author(s):  
A. Koller ◽  
D. Sun ◽  
E. J. Messina ◽  
G. Kaley
Keyword(s):  
Dependent Manner ◽  
Nitric Oxide Synthesis ◽  
Buffer Solution ◽  
Bicarbonate Buffer ◽  
Basal Diameter ◽  
Vasoactive Substances ◽  
Before And After ◽  
Dose Dependent ◽  
Intravascular Pressure

The effects of arginine analogues, inhibitors of endothelium-derived nitric oxide synthesis, on dilation of arterioles in response to various vasoactive substances were studied. At 65 mmHg intravascular pressure, isolated arterioles of rat cremaster muscle developed tone spontaneously and achieved control diameters similar to those observed in vivo (84.1 +/- 2.0 microns vs. passive diameter: 161.3 +/- 3.4 microns). Acetylcholine (ACh, 5 x 10(-8) M), sodium nitroprusside (SNP, 5 x 10(-8) M), arachidonic acid (AA, 10(-7) M), prostaglandin E2 (PGE2, 10(-9) M), and adenosine (ADO, 10(-6) M) were added to the Krebs bicarbonate buffer solution, suffusing the vessels. The peak vasodilator effects of all agents were studied before and after the administration of various doses of N omega-nitro-L-arginine (L-NNA; 10(-5), 10(-4), and 10(-3) M), which significantly reduced, in a dose-dependent manner, the basal diameter of arterioles by 3.6, 15.2, and 18.9%, respectively. The lowest concentration of L-NNA significantly inhibited arteriolar dilations to ACh by approximately 26%. Higher concentrations of L-NNA and N omega-monomethyl-L-arginine (L-NMMA; 10(-4) M) caused a further significant reduction in the dilation to ACh (to approximately 47%) and also significantly reduced dilator responses to AA and PGE2. In the presence of the highest concentration of L-NNA (10(-3) M), dilation to SNP and ADO were also significantly reduced. Removal of endothelium abolished dilation to ACh and AA but did not alter that to SNP, PGE2, or ADO.(ABSTRACT TRUNCATED AT 250 WORDS)

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