scholarly journals Cardiovascular responses to nonrespiratory and respiratory arousals in a porcine model

2001 ◽  
Vol 90 (1) ◽  
pp. 114-120 ◽  
Author(s):  
Sandrine H. Launois ◽  
Nathan Averill ◽  
Joseph H. Abraham ◽  
Debra A. Kirby ◽  
J. Woodrow Weiss
Keyword(s):  
Porcine Model ◽  
Sleep Stage ◽  
Cardiovascular Responses ◽  
Hemodynamic Response ◽  
Rapid Eye Movement Sleep ◽  
Sleep State ◽  
Renal Vasoconstriction ◽  
Airway Occlusion ◽  
Arterial Blood ◽  
Renal Vascular

Spontaneous and provoked nonrespiratory arousals can be accompanied by a patterned hemodynamic response. To investigate whether a patterned response is also elicited by respiratory arousals, we compared nonrespiratory arousals (NRA) to respiratory arousals (RA) induced by airway occlusion during non-rapid eye movement sleep. We monitored mean arterial blood pressure (MAP), heart rate, iliac and renal blood flow, and sleep stage in 7 pigs during natural sleep. Iliac and renal vascular resistance were calculated. Airway occlusions were obtained by manually inflating a chronically implanted tracheal balloon during sleep. The balloon was quickly deflated as soon as electroencephalogram arousal occurred. As previously reported, NRA generally elicited iliac vasodilation, renal vasoconstriction, little change in MAP, and tachycardia. In contrast, RA generally elicited iliac and renal vasoconstriction, an increase in MAP and tachycardia. The frequent occurrence of iliac vasoconstriction and arterial pressure elevation following RA but not NRA suggests that sleep state change alone does not account for the hemodynamic response to airway occlusion during sleep.

scholarly journals Muscle mechanoreflex activation via passive calf stretch causes renal vasoconstriction in healthy humans

2017 ◽  
Vol 312 (6) ◽  
pp. R956-R964 ◽  
Author(s):  
Rachel C. Drew ◽  
Cheryl A. Blaha ◽  
Michael D. Herr ◽  
Ruda Cui ◽  
Lawrence I. Sinoway
Keyword(s):  
Voluntary Contraction ◽  
Lower Limbs ◽  
Renal Vasoconstriction ◽  
Healthy Humans ◽  
Arterial Blood ◽  
Vasoconstrictor Response ◽  
Muscle Mechanoreflex ◽  
Metabolite Accumulation ◽  
Young Subjects ◽  
Renal Vascular

Reflex renal vasoconstriction occurs during exercise, and renal vasoconstriction in response to upper-limb muscle mechanoreflex activation has been documented. However, the renal vasoconstrictor response to muscle mechanoreflex activation originating from lower limbs, with and without local metabolite accumulation, has not been assessed. Eleven healthy young subjects (26 ± 1 yr; 5 men) underwent two trials involving 3-min passive calf muscle stretch (mechanoreflex) during 7.5-min lower-limb circulatory occlusion (CO). In one trial, 1.5-min 70% maximal voluntary contraction isometric calf exercise preceded CO to accumulate metabolites during CO and stretch (mechanoreflex and metaboreflex; 70% trial). A control trial involved no exercise before CO (mechanoreflex alone; 0% trial). Beat-to-beat renal blood flow velocity (RBFV; Doppler ultrasound), mean arterial blood pressure (MAP; photoplethysmographic finger cuff), and heart rate (electrocardiogram) were recorded. Renal vascular resistance (RVR), an index of renal vasoconstriction, was calculated as MAP/RBFV. All baseline cardiovascular variables were similar between trials. Stretch increased RVR and decreased RBFV in both trials (change from CO with stretch: RVR – 0% trial = Δ 10 ± 2%, 70% trial = Δ 7 ± 3%; RBFV – 0% trial = Δ −3.8 ± 1.1 cm/s, 70% trial = Δ −2.7 ± 1.5 cm/s; P < 0.05 for RVR and RBFV). These stretch-induced changes were of similar magnitudes in both trials, e.g., with and without local metabolite accumulation, as well as when thromboxane production was inhibited. These findings suggest that muscle mechanoreflex activation via passive calf stretch causes renal vasoconstriction, with and without muscle metaboreflex activation, in healthy humans.

Fetal breathing, sleep state, and cardiovascular responses to graded anemia in sheep

1987 ◽  
Vol 63 (4) ◽  
pp. 1463-1468 ◽  
Author(s):  
B. J. Koos ◽  
H. Sameshima ◽  
G. G. Power
Keyword(s):  
Eye Movements ◽  
Cardiovascular Responses ◽  
Severe Anemia ◽  
Sleep State ◽  
Fetal Sheep ◽  
Rapid Eye Movements ◽  
Mild Anemia ◽  
Arterial Blood ◽  
Moderate Anemia ◽  
Pressure Changes

Graded anemia was produced for 2 h in 10 unanesthetized fetal sheep by infusing plasma in exchange for fetal blood. This reduced the mean fetal hematocrits during the 1st h of anemia to 19.7 +/- 0.5% [control (C) = 28.2 +/- 1.1%] for mild anemia, 17.4 +/- 0.9% (C = 30.0 +/- 1.1%) for moderate anemia, and 15.1 +/- 1.0% (C = 29.2 +/- 1.3%) for severe anemia. The respective mean arterial O2 contents (CaO2) were 4.46 +/- 0.20, 3.89 +/- 0.24, and 3.22 +/- 0.19 ml/dl. Mean arterial PO2 was reduced significantly (by 2 Torr) only during moderate anemia, and mean arterial pH was decreased only during severe anemia. No significant changes occurred in arterial PCO2. Fetal tachycardia occurred during anemia. Mean arterial pressure was reduced by 2–3 mmHg during mild anemia; however, no significant blood pressure changes were observed for moderate or severe anemia. The incidence of rapid-eye movements and breathing activity was not affected by mild anemia, but the incidence of both was reduced significantly during moderate and severe anemia. It is concluded that 1) a reduction in CaO2 of greater than 2.48 +/- 0.22 ml/dl by hemodilution inhibits rapid-eye movements and breathing activity, and 2) the PO2 signal for inhibition does not come from arterial blood but from lower PO2 in tissue.

scholarly journals Aging augments renal vasoconstrictor response to orthostatic stress in humans

2015 ◽  
Vol 309 (12) ◽  
pp. R1474-R1478 ◽  
Author(s):  
Christine M. Clark ◽  
Kevin D. Monahan ◽  
Rachel C. Drew
Keyword(s):  
Blood Flow ◽  
Healthy Aging ◽  
Lower Body Negative Pressure ◽  
Systemic Circulation ◽  
Young Group ◽  
Orthostatic Stress ◽  
Renal Vasoconstriction ◽  
Arterial Blood ◽  
Vasoconstrictor Response ◽  
Renal Vascular

The ability of the human body to maintain arterial blood pressure (BP) during orthostatic stress is determined by several reflex neural mechanisms. Renal vasoconstriction progressively increases during graded elevations in lower body negative pressure (LBNP). This sympathetically mediated response redistributes blood flow to the systemic circulation to maintain BP. However, how healthy aging affects the renal vasoconstrictor response to LBNP is unknown. Therefore, 10 young (25 ± 1 yr; means ± SE) and 10 older (66 ± 2 yr) subjects underwent graded LBNP (−15 and −30 mmHg) while beat-to-beat renal blood flow velocity (RBFV; Doppler ultrasound), arterial BP (Finometer), and heart rate (HR; electrocardiogram) were recorded. Renal vascular resistance (RVR), an index of renal vasoconstriction, was calculated as mean BP/RBFV. All baseline cardiovascular variables were similar between groups, except diastolic BP was higher in older subjects ( P < 0.05). Increases in RVR during LBNP were greater in the older group compared with the young group (older: −15 mmHg Δ10 ± 3%, −30 mmHg Δ20 ± 5%; young: −15 mmHg Δ2 ± 2%, −30 mmHg Δ6 ± 2%; P < 0.05). RBFV tended to decrease more ( P = 0.10) and mean BP tended to decrease less ( P = 0.09) during LBNP in the older group compared with the young group. Systolic and diastolic BP, pulse pressure, and HR responses to LBNP were similar between groups. These findings suggest that aging augments the renal vasoconstrictor response to orthostatic stress in humans.

Changes in forearm muscle temperature alter renal vascular responses to isometric handgrip

2007 ◽  
Vol 293 (6) ◽  
pp. H3432-H3439 ◽  
Author(s):  
Nathan T. Kuipers ◽  
Charity L. Sauder ◽  
Matthew L. Kearney ◽  
Chester A. Ray
Keyword(s):  
Thermal Conditions ◽  
Muscle Temperature ◽  
Experimental Protocol ◽  
Isometric Handgrip ◽  
Vascular Responses ◽  
Renal Vasoconstriction ◽  
Heating And Cooling ◽  
Arterial Blood ◽  
Muscle Ischemia ◽  
Renal Vascular

The purpose of the present study was to examine the effect of heating and cooling the forearm muscles on renal vascular responses to ischemic isometric handgrip (IHG). It was hypothesized that heating and cooling the forearm would augment and attenuate, respectively, renal vascular responses to IHG. Renal vascular responses to IHG were studied during forearm heating at 39°C ( n = 15, 26 ± 1 yr) and cooling at 26°C ( n = 12, 26 ± 1 yr). For a control trial, subjects performed the experimental protocol while the forearm was normothermic (∼34°C). Muscle temperature (measured by intramuscular probe) was controlled by changing the temperature of water cycling through a water-perfused sleeve. The experimental protocol was as follows: 3 min at baseline, 1 min of ischemia, ischemic IHG to fatigue, and 2 min of postexercise muscle ischemia. At rest, renal artery blood velocity (RBV; Doppler ultrasound) and renal vascular conductance (RVC = RBV/mean arterial blood pressure) were not different between normothermia and the two thermal conditions. During ischemic IHG, there were greater decreases in RBV and RVC in the heating trial. However, RBV and RVC were similar during postexercise muscle ischemia during heating and normothermia. RVC decreased less during cooling than in normothermia while the subjects performed the ischemic IHG protocol. During postexercise muscle ischemia, RVC was greater during cooling than in normothermia. These results indicate that heating augments mechanoreceptor-mediated renal vasoconstriction whereas cooling blunts metaboreceptor-mediated renal vasoconstriction.

Myogenic contribution to agonist-induced renal vasoconstriction during normoxia and hypoxia

1997 ◽  
Vol 272 (4) ◽  
pp. H1945-H1951 ◽  
Author(s):  
M. R. Eichinger ◽  
J. M. Resta ◽  
B. R. Walker
Keyword(s):  
Renal Artery ◽  
Vascular Resistance ◽  
Acute Hypoxia ◽  
Renal Perfusion ◽  
Renal Vascular Resistance ◽  
Left Renal Artery ◽  
Sprague Dawley ◽  
Renal Vasoconstriction ◽  
Arterial Blood ◽  
Renal Vascular

Acute hypoxia attenuates agonist-induced constrictor and pressor responses in conscious rats, and a recent report suggests that hypoxia may also diminish myogenic reactivity in isolated, perfused rat kidneys. Thus we hypothesized that the diminished responsiveness to pressor agents during hypoxia is caused by an impairment of myogenic reactivity. Male Sprague-Dawley rats were instrumented with a pulsed Doppler flow probe on the left renal artery, an aortic vascular occluder cuff immediately above the left renal artery to control renal perfusion pressure, and catheters were inserted to measure systemic arterial blood pressure and renal arterial pressure (RAP) and for administration of agents. Animals were studied under normoxic or acute hypoxic (fractional concentration of O2 in inspired gials = 0.12) conditions and were administered phenylephrine, arginine vasopressin, or angiotensin II. To determine the myogenic (pressure-dependent) component of agonist-induced vasoconstriction, renal vascular resistance was calculated during agonist infusion with RAP uncontrolled and with RAP controlled to preinfusion levels. Significant myogenic components of agonist-induced renal vasoconstriction were evident with all pressor agents used. However, hypoxia did not attenuate agonist-induced, pressure-dependent increases in renal vascular resistance. We conclude that the reduced vasoreactivity associated with acute hypoxia is not caused by diminished myogenic reactivity.

scholarly journals Angiotensin II and the Renal Hemodynamic Response to an Isolated Increased Renal Venous Pressure in Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaohua Huang ◽  
Shereen M. Hamza ◽  
Wenqing Zhuang ◽  
William A. Cupples ◽  
Branko Braam
Keyword(s):  
Angiotensin Ii ◽  
Ace Inhibitor ◽  
Venous Pressure ◽  
Ace Inhibition ◽  
Hemodynamic Response ◽  
Systemic Effect ◽  
Ang Ii ◽  
Renal Vasoconstriction ◽  
Renal Hemodynamic ◽  
Renal Vascular

Elevated central venous pressure increases renal venous pressure (RVP) which can affect kidney function. We previously demonstrated that increased RVP reduces renal blood flow (RBF), glomerular filtration rate (GFR), and renal vascular conductance (RVC). We now investigate whether the RAS and RBF autoregulation are involved in the renal hemodynamic response to increased RVP. Angiotensin II (ANG II) levels were clamped by infusion of ANG II after administration of an angiotensin-converting enzyme (ACE) inhibitor in male Lewis rats. This did not prevent the decrease in ipsilateral RBF (−1.9±0.4ml/min, p&lt;0.05) and GFR (−0.77±0.18ml/min, p&lt;0.05) upon increased RVP; however, it prevented the reduction in RVC entirely. Systemically, the RVP-induced decline in mean arterial pressure (MAP) was more pronounced in ANG II clamped animals vs. controls (−22.4±4.1 vs. −9.9±2.3mmHg, p&lt;0.05), whereas the decrease in heart rate (HR) was less (−5±6bpm vs. −23±4bpm, p&lt;0.05). In animals given vasopressin to maintain a comparable MAP after ACE inhibition (ACEi), increased RVP did not impact MAP and HR. RVC also did not change (0.018±0.008ml/minˑmmHg), and the reduction of GFR was no longer significant (−0.54±0.15ml/min). Furthermore, RBF autoregulation remained intact and was reset to a lower level when RVP was increased. In conclusion, RVP-induced renal vasoconstriction is attenuated when ANG II is clamped or inhibited. The systemic effect of increased RVP, a decrease in HR related to a mild decrease in blood pressure, is attenuated also during ANG II clamp. Last, RBF autoregulation remains intact when RVP is elevated and is reduced to lower levels of RBF. This suggests that in venous congestion, the intact RBF autoregulation could be partially responsible for the vasoconstriction.

ET-3 is extracted by and induces potent vasoconstriction in human splanchnic and renal vasculatures

1995 ◽  
Vol 79 (4) ◽  
pp. 1255-1259 ◽  
Author(s):  
E. Weitzberg ◽  
A. Hemsen ◽  
J. M. Lundberg ◽  
G. Ahlborg
Keyword(s):  
Receptor Activation ◽  
Vascular Effects ◽  
Renal Vasoconstriction ◽  
Blood Flows ◽  
Arterial Blood ◽  
Etb Receptor ◽  
Vascular Beds ◽  
Arterial Plasma ◽  
Endothelin 3 ◽  
Renal Vascular

To investigate splanchnic and renal vascular effects and elimination of endothelin-3 (ET-3), ET-3 (10 pmol.kg-1.min-1 iv for 20 min) was given to six healthy male volunteers. Arterial plasma ET-3-like immunoreactivity (ET-3-Li) increased 10-fold to 111 +/- 31 pmol/l (P < 0.01). The initial half-life of plasma ET-3-Li determined in three subjects was 1.7 +/- 0.2 min. The fractional extraction of ET-3-Li was 68 +/- 7% in the splanchnic and 63 +/- 4% in the renal vascular beds. Mean arterial blood pressure fell from 86 +/- 4 to 94 +/- 4 mmHg (10%) (P < 0.05). Splanchnic and renal blood flows fell by 43 +/- 3% (P < 0.05) and 29 +/- 4% (P < 0.05), respectively, during the infusion. Splanchnic and renal vascular resistances rose by 92 +/- 22% (P < 0.05) and 58 +/- 7% (P < 0.05). In conclusion, ET-3 infusion in humans induces splanchnic and renal vasoconstriction of similar magnitude as previously shown during endothelin-1 infusion, presumably by ETB receptor activation. Plasma ET-3 is efficiently extracted in the splanchnic and renal vascular regions.

scholarly journals Influence of sex and active muscle mass on renal vascular responses during static exercise

2006 ◽  
Vol 291 (1) ◽  
pp. H121-H126 ◽  
Author(s):  
Afsana Momen ◽  
Brian Handly ◽  
Allen Kunselman ◽  
Urs A. Leuenberger ◽  
Lawrence I. Sinoway
Keyword(s):  
Blood Flow ◽  
Muscle Mass ◽  
Maximum Voluntary Contraction ◽  
Duplex Ultrasound ◽  
Cardiovascular Responses ◽  
Voluntary Contraction ◽  
Static Exercise ◽  
Men And Women ◽  
Renal Vasoconstriction ◽  
Renal Vascular

During exercise, reflex renal vasoconstriction helps maintain blood pressure and redistributes blood flow to the contracting muscle. Sex and muscle mass have been shown to influence certain cardiovascular responses to exercise. Whether sex and/or muscle mass influence renal vasoconstrictor responses to exercise is unknown. We studied healthy men ( n = 10) and women ( n = 10) matched for age and body mass index during handgrip (HG, small muscle mass) and quadriceps contraction (QC, large muscle mass) as beat-to-beat changes in renal blood flow velocity (RBV; duplex ultrasound), mean arterial pressure (MAP; Finapres), and heart rate (ECG) were monitored. Renal vascular resistance (RVR) index was calculated as MAP ÷ RBV. Responses to HG vs. QC were compared in 13 subjects. We found that 1) RVR responses to short (15-s) bouts and fatiguing HG were similar in men and women (change in RVR during 15-s HG at 70% of maximum voluntary contraction = 23 ± 4 and 31 ± 4% in men and women, respectively, P = not significant); 2) post-HG circulatory responses were similar in men and women; and 3) HG and QC were similar during short (15-s) bouts (change in RVR during HG at 50% of maximum voluntary contraction = 19 ± 3 and 18 ± 5% for arm and leg, respectively, P = not significant). Our findings suggest that muscle reflex-mediated renal vasoconstriction is similar in men and women during static exercise. Moreover, muscle mass does not contribute to the magnitude of the reflex renal vasoconstrictor response seen with muscle contraction.

ETA receptors mediate vasoconstriction, whereas ETB receptors clear endothelin-1 in the splanchnic and renal circulation of healthy men

2003 ◽  
Vol 104 (2) ◽  
pp. 143-151 ◽  
Author(s):  
Felix BÖHM ◽  
John PERNOW ◽  
Jonas LINDSTRÖM ◽  
Gunvor AHLBORG
Keyword(s):  
Receptor Antagonist ◽  
Vascular Resistance ◽  
Vascular Tone ◽  
Renal Vasoconstriction ◽  
Healthy Humans ◽  
Arterial Blood ◽  
Eta Receptor ◽  
Etb Receptor ◽  
Eta Receptor Antagonist ◽  
Renal Vascular

The contribution of the endothelin (ET) receptors ETA and ETB to basal vascular tone and ET-1-induced vasoconstriction in the renal and splanchnic vasculature was investigated in six healthy humans. ET-1 was infused alone and in combination with the selective ETA receptor antagonist BQ123 or the selective ETB receptor antagonist BQ788 on three different occasions. BQ123 did not affect basal arterial blood pressure, splanchnic vascular resistance (SplVR) or renal vascular resistance (RVR), but inhibited the increase in vascular resistance induced by ET-1 [64±18 versus -1±7% in SplVR (P<0.05); 36±6 versus 12±3% in RVR (P<0.0001)]. BQ788 increased basal SplVR and RVR [38±16% (P = 0.01) and 21±5% (P<0.0001) respectively], and potentiated the ET-1-induced vasoconstriction. Plasma ET-1 increased more after ETB blockade than under control conditions or after ETA blockade. These findings suggest that the ETA receptor mediates the splanchnic and renal vasoconstriction induced by ET-1 in healthy humans. The ETB receptor seems to function as a clearance receptor and may modulate vascular tone by altering the plasma concentration of ET-1.

scholarly journals Effect of healthy aging on renal vascular responses to local cooling and apnea

2013 ◽  
Vol 115 (1) ◽  
pp. 90-96 ◽  
Author(s):  
Hardikkumar M. Patel ◽  
Jessica L. Mast ◽  
Lawrence I. Sinoway ◽  
Matthew D. Muller
Keyword(s):  
Older Adults ◽  
Healthy Aging ◽  
Pain Perception ◽  
Pressor Response ◽  
Cold Pressor Test ◽  
Resistance Index ◽  
Local Cooling ◽  
Renal Vasoconstriction ◽  
Arterial Blood ◽  
Renal Vascular

Sympathetically mediated renal vasoconstriction may contribute to the pathogenesis of hypertension in older adults, but empirical data in support of this concept are lacking. In 10 young (26 ± 1 yr) and 11 older (67 ± 2 yr) subjects, we quantified acute hemodynamic responses to three sympathoexcitatory stimuli: local cooling of the forehead, cold pressor test (CPT), and voluntary apnea. We hypothesized that all stimuli would increase mean arterial blood pressure (MAP) and renal vascular resistance index (RVRI) and that aging would augment these effects. Beat-by-beat MAP, heart rate (HR), and renal blood flow velocity (from Doppler) were measured in the supine posture, and changes from baseline were compared between groups. In response to 1°C forehead cooling, aging was associated with an augmented MAP (20 ± 3 vs. 6 ± 2 mmHg) and RVRI (35 ± 6 vs. 16 ± 9%) but not HR. In older adults, there was a positive correlation between the cold-induced pressor response and forehead pain (R = 0.726), but this effect was not observed in young subjects. The CPT raised RVRI in both young (56 ± 13%) and older (45 ± 8%) subjects, but this was not different between groups. Relative to baseline, end-expiratory apnea increased RVRI to a similar extent in both young (46 ± 14%) and older (41 ± 9%) subjects. During sympathetic activation, renal vasoconstriction occurred in both groups. Forehead cooling caused an augmented pressor response in older adults that was related to pain perception.

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