Vascular Distribution of a Potent Vasoconstrictor Peptide, Neuropeptide Y (NPY)

1984 ◽  
Vol 66 (6) ◽  
pp. 71P.2-71P
Author(s):  
J M Allen ◽  
J C Yeats ◽  
K Darcy ◽  
A Savage ◽  
S R Bloom
Keyword(s):  
Neuropeptide Y ◽  
Potent Vasoconstrictor ◽  
Vasoconstrictor Peptide

Neuropeptide Y: a novel renal peptide with vasoconstrictor and natriuretic activity

1985 ◽  
Vol 68 (4) ◽  
pp. 373-377 ◽  
Author(s):  
J. M. Allen ◽  
A. E. G. Raine ◽  
J. G. G. Ledingham ◽  
S. R. Bloom
Keyword(s):  
Neuropeptide Y ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Juxtaglomerular Apparatus ◽  
Renal Perfusion ◽  
Sodium Reabsorption ◽  
Potent Vasoconstrictor ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Vasoconstrictor Peptide

1. A novel vasoconstrictor peptide, neuropeptide Y (NPY), has been identified in considerable quantities in the renal artery and kidney. Within the kidney, NPY was confined to the cortex and corticomedullary interface, the regions where the juxtaglomerular apparatus is most numerous. 2. In the isolated perfused rat kidney, NPY caused a prompt dose-dependent increase in perfusion pressure and reduction in flow, with only a small fall in glomerular filtration rate (GFR). In spite of the reduced renal perfusion, a dose-dependent natriuresis was observed. This response contrasts to the response of this preparation to noradrenaline, which causes sodium reabsorption. 3. The presence of a potent vasoconstrictor and natriuretic peptide within the rat renovascular system suggests that it may play a significant role in the control of renal function.

Vascular Distribution of a Potent Vasoconstrictor Peptide, Neuropeptide Y (Npy)

1984 ◽  
Vol 66 (2) ◽  
pp. 71P-71P
Author(s):  
J M Allen ◽  
J C Yeats ◽  
K Darcy ◽  
A Savage ◽  
S R Bloom
Keyword(s):  
Neuropeptide Y ◽  
Potent Vasoconstrictor ◽  
Vasoconstrictor Peptide

Does endoplasmic reticulum stress mediate endothelin-1-induced renal inflammation?

2013 ◽  
Vol 305 (2) ◽  
pp. R107-R109 ◽  
Author(s):  
Carmen De Miguel ◽  
Jennifer S. Pollock
Keyword(s):  
Endoplasmic Reticulum ◽  
Thick Ascending Limb ◽  
Afferent Arteriole ◽  
Renal Vasculature ◽  
Renal Inflammation ◽  
Endothelin 1 ◽  
Collecting Ducts ◽  
Potent Vasoconstrictor ◽  
Eventual Death ◽  
Vasoconstrictor Peptide

Endothelin-1 (ET-1) is the most potent vasoconstrictor peptide known. It exerts its actions through two pharmacologically different receptors: ETA and ETB receptors. In the renal vasculature, there is a majority of ETB receptors in the efferent arteriole, whereas a greater amount of ETA receptors are located in the afferent arteriole. The nephron is rich in ETB receptors, especially in the thick ascending limb and collecting ducts, while containing a smaller amount of ETA receptors. High levels of circulating or renal ET-1 have been described in cardiovascular diseases such as hypertension or diabetes, diseases also associated to renal inflammation. Despite extensive evidence associating high levels of ET-1 to increased renal inflammation, the molecular mechanism(s) by which ET-1 leads to renal immune infiltration and/or immune activation remains unknown. In this minireview, we propose that the ET-1/ETA pathway mediates an increase in renal endoplasmic reticulum (ER) stress, initially a survival mechanism that if prolonged, leads to the eventual death of the cell via apoptosis.

Tachyphylaxis to the vasopressor effects of endothelin in rat aortic rings

1993 ◽  
Vol 264 (2) ◽  
pp. H352-H356 ◽  
Author(s):  
S. M. Hollenberg ◽  
J. H. Shelhamer ◽  
R. E. Cunnion
Keyword(s):  
Endothelial Cells ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Pressor Effect ◽  
Endothelin Receptor ◽  
Surface Receptors ◽  
Receptor Complexes ◽  
High Affinity ◽  
Potent Vasoconstrictor ◽  
Vasoconstrictor Peptide

Endothelin-1 (ET-1), a potent vasoconstrictor peptide released by endothelial cells, binds with high affinity to surface receptors and is highly resistant to dissociation. We observed tachyphylaxis to the pressor effects of a second application of ET-1 in rat aortic rings and investigated the mechanism of this effect. Developed tension increased progressively with doses of ET-1 ranging from 1 to 500 nM (P < 0.001), and tensions with rechallenge were correspondingly decreased (P < 0.001). In response to 500 nM ET-1, tension increased 1,599 +/- 72 (SE) mg/mg ring wt. Rechallenge with 500 nM ET-1 led to contraction of only 33 +/- 40 mg/mg ring wt. Tachyphylaxis was seen up to 6 h after initial challenge. Pretreatment with nicardipine, lidoflazine, nitroglycerin, and sphingosine did not affect tachyphylaxis. Pretreatment with 500 microM dansylcadaverine (an inhibitor of endothelin internalization) markedly inhibited ET-1-induced contraction and also inhibited tachyphylaxis to ET-1. Further studies with radiolabeled ET-1 suggested that subsequent ET-1 binding is markedly decreased after an initial ET-1 challenge. Dansylcadaverine inhibited ET-1 internalization and also inhibited the decreased binding seen with ET-1 rechallenge. Rat aortic rings demonstrate tachyphylaxis to the pressor effect of a second dose of ET-1. The mechanism appears to be related to binding and subsequent internalization of endothelin-receptor complexes. This effect suggests a possible mechanism for sustained decreases in systemic vascular resistance.

Suppression of baroreceptor discharge by endothelin at high carotid sinus pressure

1992 ◽  
Vol 263 (1) ◽  
pp. R103-R108 ◽  
Author(s):  
M. W. Chapleau ◽  
G. Hajduczok ◽  
F. M. Abboud
Keyword(s):  
Endothelial Cells ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
High Dose ◽  
Nerve Activity ◽  
Local Exposure ◽  
Potent Vasoconstrictor ◽  
Alpha Chloralose ◽  
Vasoconstrictor Peptide ◽  
Sinus Pressure

Endothelin is a potent vasoconstrictor peptide released from endothelial cells capable of producing marked and prolonged increases in arterial pressure. The purpose of this study was to determine whether endothelin alters the sensitivity of arterial baroreceptors. Multifiber baroreceptor activity was recorded from the vascularly isolated, endothelium-denuded carotid sinus in dogs anesthetized with alpha-chloralose. Local exposure of baroreceptors to endothelin at a concentration of 10(-8) M produced vasoconstriction of the carotid sinus as measured with sonomicrometer crystals but did not alter baroreceptor discharge significantly. A higher concentration of endothelin (10(-7) M) markedly suppressed baroreceptor activity, particularly at pressures greater than 100 mmHg (n = 7, P less than 0.05). The magnitude of the decrease in activity was dependent on the duration of exposure to endothelin. Baroreceptor activity measured at carotid pressures of 60, 100, and 200 mmHg averaged 23 +/- 4, 65 +/- 6, and 100 +/- 0% of maximum during control; 38 +/- 12, 61 +/- 9, and 74 +/- 15% after exposure to endothelin (10(-7) M) for 2 min; and 27 +/- 8, 53 +/- 12, and 56 +/- 19% after 12 min, respectively. The suppression of nerve activity with the high dose of endothelin was not accompanied by additional vasoconstriction, suggesting a direct effect of endothelin on nerve endings. We speculate that endothelin released from endothelial cells may act in a paracrine manner to suppress activity of baroreceptors, particularly at high levels of arterial pressure. Such an action would interfere with the buffering capacity of the baroreflex and promote hypertension.

scholarly journals Effect of neuropeptide Y on hemodynamics of the rabbit lung

1998 ◽  
Vol 84 (2) ◽  
pp. 618-623 ◽  
Author(s):  
Sally A. Lang ◽  
Michael B. Maron
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Neuropeptide Y ◽  
Rabbit Lung ◽  
Vasoactive Agent ◽  
Arterial Resistance ◽  
Pulmonary Capillary ◽  
Intact Rabbit ◽  
Sympathetic Nervous ◽  
Potent Vasoconstrictor

Lang, Sally A., and Michael B. Maron.Effect of neuropeptide Y on hemodynamics of the rabbit lung. J. Appl. Physiol. 84(2): 618–623, 1998.—We evaluated the effect of neuropeptide Y (NPY) on the hemodynamics of the isolated rabbit lung perfused at constant flow and outflow pressure. Doses of 10−8 and 10− 7 M NPY increased pulmonary arterial pressure (Ppa) from 11.5 ± 1.0 (SE) mmHg to, respectively, 16.4 ± 1.5 and 26.0 ± 3.8 mmHg ( P < 0.05, n = 5 mmHg lungs), with 78 ± 4% of the increase at 10−7 M resulting from an increased arterial resistance. At the latter dose, pulmonary capillary pressure increased from 5.8 ± 0.9 to 9.4 ± 1.0 mmHg ( P < 0.05). When administered in the presence of norepinephrine, 10−8 and 10−7 M NPY ( n = 6) produced extreme increases in Ppa to 66.1 ± 20.5 and 114.7 ± 25.5 mmHg, respectively, that were due primarily to an increased arterial resistance. To determine the significance of circulating NPY as a pulmonary vasoactive agent, we measured plasma NPY-like immunoreactivity in anesthetized rabbits after massively activating the sympathetic nervous system with veratrine. NPY-like immunoreactivity increased from 74 ± 10 to 111 ± 10 (SE) pM ( P < 0.05). Thus, although NPY is a potent vasoconstrictor in the rabbit lung, it is not likely that plasma NPY concentrations rise sufficiently, even after massive sympathetic nervous system activation, to produce pulmonary vasoconstriction in the intact rabbit.

Endothelin-1 vasoconstriction and the age-related decline in endothelium-dependent vasodilatation in men

2011 ◽  
Vol 120 (11) ◽  
pp. 485-491 ◽  
Author(s):  
Christian M. Westby ◽  
Brian R. Weil ◽  
Jared J. Greiner ◽  
Brian L. Stauffer ◽  
Christopher A. Desouza
Keyword(s):  
Young Men ◽  
Older Men ◽  
Endothelin 1 ◽  
Age Related ◽  
Eta Receptor ◽  
Vasomotor Regulation ◽  
Artery Disease ◽  
Potent Vasoconstrictor ◽  
Vasoconstrictor Peptide

ET (endothelin)-1, a potent vasoconstrictor peptide released by the endothelium, plays an important role in vasomotor regulation and has been linked to diminished endothelial vasodilator capacity in several pathologies associated with human aging, including hypertension, Type 2 diabetes and coronary artery disease. However, it is currently unknown whether the decline in endothelial vasodilatation with advancing age is due to elevated ET-1 vasconstrictor activity. Accordingly, we tested the hypothesis that the age-related impairment in ACh (acetylcholine)-mediated endothelium-dependent vasodilatation is due, at least in part, to increased ET-1-mediated vasoconstrictor tone. FBF (forearm blood flow) responses to ACh, SNP (sodium nitroprusside) and BQ-123 (ETA receptor blocker) were determined in 14 young (age, 25±1 years) and 14 older (age, 61±2 years) healthy non-obese men. Additionally, FBF responses to ACh were determined in the presence of ETA blockade. Vasodilatation to ACh was lower (approx. 25%; P<0.05) in the older men (from 4.9±0.2 to 13.9±0.9 ml·100 ml−1 of tissue·min−1) compared with the young men (4.6±0.3 to 17.2±1.0 ml·100 ml−1 of tissue·min−1). There were no differences in FBF responses to SNP between the young (4.8±0.3 to 18.5±0.3 ml·100 ml−1 of tissue·min−1) and older (5.1±0.3 to 17.3±0.8 ml·100 ml−1 of tissue·min−1) men. In the young men, resting FBF was not significantly altered by BQ-123, whereas, in the older men, FBF increased approx. 25% in response to BQ-123 infusion (P<0.05). Co-infusion of ACh with BQ-123 resulted in an approx. 20% increase in the ACh-induced vasodilatation in older men compared with saline. In contrast, FBF responses to ACh were not significantly altered by ETA blockade in the young men. In conclusion, these results demonstrate that ET-1 vasoconstrictor activity contributes, at least in part, to diminished endothelium-dependent vasodilatation in older men.

Kasstasin: A novel potent vasoconstrictor peptide from the skin secretion of the African red-legged running frog, Kassina maculata

Biochimie ◽  
2011 ◽  
Vol 93 (9) ◽  
pp. 1537-1542 ◽  
Author(s):  
Xiaohe Li ◽  
Wanyu Feng ◽  
Mei Zhou ◽  
Chengbang Ma ◽  
Tianbao Chen ◽  
...  
Keyword(s):  
Skin Secretion ◽  
Potent Vasoconstrictor ◽  
Vasoconstrictor Peptide

scholarly journals A novel potent vasoconstrictor peptide produced by vascular endothelial cells

Nature ◽  
1988 ◽  
Vol 332 (6163) ◽  
pp. 411-415 ◽  
Author(s):  
Masashi Yanagisawa ◽  
Hiroki Kurihara ◽  
Sadao Kimura ◽  
Yoko Tomobe ◽  
Mieko Kobayashi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Potent Vasoconstrictor ◽  
Vasoconstrictor Peptide

scholarly journals Neuropeptide Y: Sympathetic Cotransmitter and Modulator?

Physiology ◽  
1989 ◽  
Vol 4 (1) ◽  
pp. 13-17 ◽  
Author(s):  
JM Lundberg ◽  
J Pernow ◽  
JS Lacroix
Keyword(s):  
Neuropeptide Y ◽  
Nerve Stimulation ◽  
High Frequency ◽  
Sympathetic Nerves ◽  
Sympathetic Stimulation ◽  
Vascular Control ◽  
Perivascular Nerves ◽  
Potent Vasoconstrictor ◽  
High Degree

Neuropeptide Y (NPY) exerts potent vasoconstrictor activity and is coreleased with noradrenaline from sympathetic nerves, mainly on a high degree of activation. It may contribute to the vasoconstriction on high-frequency sympathetic stimulation during control conditions and mediate the long-lasting responses evoked by nerve stimulation in the absence of noradrenaline. NPY enhances the vasomotor effects to noradrenaline and inhibits its release from perivascular nerves. NPY probably is a cotransmitter in sympathetic vascular control.

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