The fibrinolytic system attenuates vascular tone: effects of tissue plasminogen activator (tPA) and aminocaproic acid on renal microcirculation
The renal medulla is a major source of plasminogen activators (PA), recently shown to induce vasodilation in vitro. Treatment with PA inhibitors has been associated with renal dysfunction, suggesting compromised renal microvasculature. We investigated the impact of the PA inhibitor epsilon amino‐cap...
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| Published in: | British journal of pharmacology Vol. 141; no. 6; pp. 971 - 978 |
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| Main Authors: | , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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Blackwell Publishing Ltd
01-03-2004
Nature Publishing |
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| Abstract | The renal medulla is a major source of plasminogen activators (PA), recently shown to induce vasodilation in vitro. Treatment with PA inhibitors has been associated with renal dysfunction, suggesting compromised renal microvasculature. We investigated the impact of the PA inhibitor epsilon amino‐caproic acid (EACA) upon vascular tone in vitro, and studied the effect of both tPA and EACA upon intrarenal hemodynamics in vivo.
In vitro experiments were carried out in isolated aortic rings and with cultured vascular smooth muscle cells. Studies of renal microcirculation and morphology were conducted in anesthetized Sprague–Dawley rats.
In isolated aortic rings, EACA (but not the other inhibitors of the fibrinolytic system PAI‐1 or α‐2 antiplasmin) reduced the half‐maximal effective concentration of phenylephrine (PE) required to induce contraction (from 32 nM in control solution to 2 and 0.1 nM at EACA concentrations of 1 and 10 μM, respectively). Using reteplase (retavase) in the same model, we also provide evidence that the vasoactivity of tPA is in part kringle‐dependent. In cultured vascular smooth muscle cells, Ca2+ internalization following PE was enhanced by EACA, and retarded by tPA.
In anesthetized rats, EACA (150 mg kg−1) did not affect systemic blood pressure, total renal or cortical blood flow. However, the outer medullary blood flow declined 12±2% below the baseline (P<0.03). By contrast, tPA (2 mg kg−1), transiently increased outer medullary blood flow by 8±5% (P<0.02). Fibrin microthrombi were not found within the renal microvasculature in EACA‐treated animals.
In conclusion, both fibrinolytic and antifibrinolytic agents modulate medullary renal blood flow with reciprocal effects of vasodilation (PA) and vasoconstriction (EACA). In vitro studies suggest that these hemodynamic responses are related to direct modulation of the vascular tone.
British Journal of Pharmacology (2004) 141, 971–978. doi:10.1038/sj.bjp.0705714 |
|---|---|
| AbstractList | The renal medulla is a major source of plasminogen activators (PA), recently shown to induce vasodilation
in vitro
. Treatment with PA inhibitors has been associated with renal dysfunction, suggesting compromised renal microvasculature. We investigated the impact of the PA inhibitor epsilon amino-caproic acid (EACA) upon vascular tone
in vitro
, and studied the effect of both tPA and EACA upon intrarenal hemodynamics
in vivo
.
In vitro
experiments were carried out in isolated aortic rings and with cultured vascular smooth muscle cells. Studies of renal microcirculation and morphology were conducted in anesthetized Sprague–Dawley rats.
In isolated aortic rings, EACA (but not the other inhibitors of the fibrinolytic system PAI-1 or
α
-2 antiplasmin) reduced the half-maximal effective concentration of phenylephrine (PE) required to induce contraction (from 32 n
M
in control solution to 2 and 0.1 n
M
at EACA concentrations of 1 and 10
μ
M
, respectively). Using reteplase (retavase) in the same model, we also provide evidence that the vasoactivity of tPA is in part kringle-dependent. In cultured vascular smooth muscle cells, Ca
2+
internalization following PE was enhanced by EACA, and retarded by tPA.
In anesthetized rats, EACA (150 mg kg
−1
) did not affect systemic blood pressure, total renal or cortical blood flow. However, the outer medullary blood flow declined 12±2% below the baseline (
P
<0.03). By contrast, tPA (2 mg kg
−1
), transiently increased outer medullary blood flow by 8±5% (
P
<0.02). Fibrin microthrombi were not found within the renal microvasculature in EACA-treated animals.
In conclusion, both fibrinolytic and antifibrinolytic agents modulate medullary renal blood flow with reciprocal effects of vasodilation (PA) and vasoconstriction (EACA).
In vitro
studies suggest that these hemodynamic responses are related to direct modulation of the vascular tone. 1. The renal medulla is a major source of plasminogen activators (PA), recently shown to induce vasodilation in vitro. Treatment with PA inhibitors has been associated with renal dysfunction, suggesting compromised renal microvasculature. We investigated the impact of the PA inhibitor epsilon amino-caproic acid (EACA) upon vascular tone in vitro, and studied the effect of both tPA and EACA upon intrarenal hemodynamics in vivo. 2. In vitro experiments were carried out in isolated aortic rings and with cultured vascular smooth muscle cells. Studies of renal microcirculation and morphology were conducted in anesthetized Sprague-Dawley rats. 3. In isolated aortic rings, EACA (but not the other inhibitors of the fibrinolytic system PAI-1 or alpha-2 antiplasmin) reduced the half-maximal effective concentration of phenylephrine (PE) required to induce contraction (from 32 nm in control solution to 2 and 0.1 nm at EACA concentrations of 1 and 10 microm, respectively). Using reteplase (retavase) in the same model, we also provide evidence that the vasoactivity of tPA is in part kringle-dependent. In cultured vascular smooth muscle cells, Ca(2+) internalization following PE was enhanced by EACA, and retarded by tPA. 4. In anesthetized rats, EACA (150 mg x kg(-1)) did not affect systemic blood pressure, total renal or cortical blood flow. However, the outer medullary blood flow declined 12+/-2% below the baseline (P<0.03). By contrast, tPA (2 mg x kg(-1)), transiently increased outer medullary blood flow by 8+/-5% (P<0.02). Fibrin microthrombi were not found within the renal microvasculature in EACA-treated animals. 5. In conclusion, both fibrinolytic and antifibrinolytic agents modulate medullary renal blood flow with reciprocal effects of vasodilation (PA) and vasoconstriction (EACA). In vitro studies suggest that these hemodynamic responses are related to direct modulation of the vascular tone. The renal medulla is a major source of plasminogen activators (PA), recently shown to induce vasodilation in vitro . Treatment with PA inhibitors has been associated with renal dysfunction, suggesting compromised renal microvasculature. We investigated the impact of the PA inhibitor epsilon amino‐caproic acid (EACA) upon vascular tone in vitro , and studied the effect of both tPA and EACA upon intrarenal hemodynamics in vivo . In vitro experiments were carried out in isolated aortic rings and with cultured vascular smooth muscle cells. Studies of renal microcirculation and morphology were conducted in anesthetized Sprague–Dawley rats. In isolated aortic rings, EACA (but not the other inhibitors of the fibrinolytic system PAI‐1 or α ‐2 antiplasmin) reduced the half‐maximal effective concentration of phenylephrine (PE) required to induce contraction (from 32 n M in control solution to 2 and 0.1 n M at EACA concentrations of 1 and 10 μ M , respectively). Using reteplase (retavase) in the same model, we also provide evidence that the vasoactivity of tPA is in part kringle‐dependent. In cultured vascular smooth muscle cells, Ca 2+ internalization following PE was enhanced by EACA, and retarded by tPA. In anesthetized rats, EACA (150 mg kg −1 ) did not affect systemic blood pressure, total renal or cortical blood flow. However, the outer medullary blood flow declined 12±2% below the baseline ( P <0.03). By contrast, tPA (2 mg kg −1 ), transiently increased outer medullary blood flow by 8±5% ( P <0.02). Fibrin microthrombi were not found within the renal microvasculature in EACA‐treated animals. In conclusion, both fibrinolytic and antifibrinolytic agents modulate medullary renal blood flow with reciprocal effects of vasodilation (PA) and vasoconstriction (EACA). In vitro studies suggest that these hemodynamic responses are related to direct modulation of the vascular tone. British Journal of Pharmacology (2004) 141 , 971–978. doi: 10.1038/sj.bjp.0705714 The renal medulla is a major source of plasminogen activators (PA), recently shown to induce vasodilation in vitro. Treatment with PA inhibitors has been associated with renal dysfunction, suggesting compromised renal microvasculature. We investigated the impact of the PA inhibitor epsilon amino‐caproic acid (EACA) upon vascular tone in vitro, and studied the effect of both tPA and EACA upon intrarenal hemodynamics in vivo. In vitro experiments were carried out in isolated aortic rings and with cultured vascular smooth muscle cells. Studies of renal microcirculation and morphology were conducted in anesthetized Sprague–Dawley rats. In isolated aortic rings, EACA (but not the other inhibitors of the fibrinolytic system PAI‐1 or α‐2 antiplasmin) reduced the half‐maximal effective concentration of phenylephrine (PE) required to induce contraction (from 32 nM in control solution to 2 and 0.1 nM at EACA concentrations of 1 and 10 μM, respectively). Using reteplase (retavase) in the same model, we also provide evidence that the vasoactivity of tPA is in part kringle‐dependent. In cultured vascular smooth muscle cells, Ca2+ internalization following PE was enhanced by EACA, and retarded by tPA. In anesthetized rats, EACA (150 mg kg−1) did not affect systemic blood pressure, total renal or cortical blood flow. However, the outer medullary blood flow declined 12±2% below the baseline (P<0.03). By contrast, tPA (2 mg kg−1), transiently increased outer medullary blood flow by 8±5% (P<0.02). Fibrin microthrombi were not found within the renal microvasculature in EACA‐treated animals. In conclusion, both fibrinolytic and antifibrinolytic agents modulate medullary renal blood flow with reciprocal effects of vasodilation (PA) and vasoconstriction (EACA). In vitro studies suggest that these hemodynamic responses are related to direct modulation of the vascular tone. British Journal of Pharmacology (2004) 141, 971–978. doi:10.1038/sj.bjp.0705714 1. The renal medulla is a major source of plasminogen activators (PA), recently shown to induce vasodilation in vitro. Treatment with PA inhibitors has been associated with renal dysfunction, suggesting compromised renal microvasculature. We investigated the impact of the PA inhibitor epsilon amino-caproic acid (EACA) upon vascular tone in vitro, and studied the effect of both tPA and EACA upon intrarenal hemodynamics in vivo. 2. In vitro experiments were carried out in isolated aortic rings and with cultured vascular smooth muscle cells. Studies of renal microcirculation and morphology were conducted in anesthetized Sprague-Dawley rats. 3. In isolated aortic rings, EACA (but not the other inhibitors of the fibrinolytic system PAI-1 or alpha-2 antiplasmin) reduced the half-maximal effective concentration of phenylephrine (PE) required to induce contraction (from 32 nm in control solution to 2 and 0.1 nm at EACA concentrations of 1 and 10 microm, respectively). Using reteplase (retavase) in the same model, we also provide evidence that the vasoactivity of tPA is in part kringle-dependent. In cultured vascular smooth muscle cells, Ca(2+) internalization following PE was enhanced by EACA, and retarded by tPA. 4. In anesthetized rats, EACA (150 mg x kg(-1)) did not affect systemic blood pressure, total renal or cortical blood flow. However, the outer medullary blood flow declined 12+/-2% below the baseline (P<0.03). By contrast, tPA (2 mg x kg(-1)), transiently increased outer medullary blood flow by 8+/-5% (P<0.02). Fibrin microthrombi were not found within the renal microvasculature in EACA-treated animals. 5. In conclusion, both fibrinolytic and antifibrinolytic agents modulate medullary renal blood flow with reciprocal effects of vasodilation (PA) and vasoconstriction (EACA). In vitro studies suggest that these hemodynamic responses are related to direct modulation of the vascular tone. |
| Author | Shina, Ahuva Hanna, Zohair Nassar, Taher Akkawi, Sa'ed Goldfarb, Marina Rosen, Seymour Heyman, Samuel N Higazi, Abd‐Al Roof |
| AuthorAffiliation | 2 2 Department of Biochemistry, Hadassah Hospital, Ein Kerem, Jerusalem, Israel 3 3 The Renal Unit, Bikur Holim Hospital, Jerusalem, Israel 4 4 Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, U.S.A 5 5 The Hebrew University Medical School, Jerusalem, Israel 1 1 Department of Medicine, Hadassah University Hospital, Mt Scopus, P.O. Box 24035, Jerusalem 91240, Israel |
| AuthorAffiliation_xml | – name: 1 1 Department of Medicine, Hadassah University Hospital, Mt Scopus, P.O. Box 24035, Jerusalem 91240, Israel – name: 2 2 Department of Biochemistry, Hadassah Hospital, Ein Kerem, Jerusalem, Israel – name: 4 4 Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, U.S.A – name: 3 3 The Renal Unit, Bikur Holim Hospital, Jerusalem, Israel – name: 5 5 The Hebrew University Medical School, Jerusalem, Israel |
| Author_xml | – sequence: 1 givenname: Samuel N surname: Heyman fullname: Heyman, Samuel N – sequence: 2 givenname: Zohair surname: Hanna fullname: Hanna, Zohair – sequence: 3 givenname: Taher surname: Nassar fullname: Nassar, Taher – sequence: 4 givenname: Ahuva surname: Shina fullname: Shina, Ahuva – sequence: 5 givenname: Sa'ed surname: Akkawi fullname: Akkawi, Sa'ed – sequence: 6 givenname: Marina surname: Goldfarb fullname: Goldfarb, Marina – sequence: 7 givenname: Seymour surname: Rosen fullname: Rosen, Seymour – sequence: 8 givenname: Abd‐Al Roof surname: Higazi fullname: Higazi, Abd‐Al Roof |
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| Keywords | medulla Calcium Hemostatic Rat tissue plasminogen activator Smooth muscle Aminocaproic acid Inorganic element Kidney t-Plasminogen activator Microcirculation Laser dopplerometry Blood vessel Antifibrinolytic laser Doppler vascular smooth muscle Serine endopeptidases Enzyme Rodentia Pharmacology Fibrinolysis Peptidases Vertebrata Mammalia Urinary system Animal Reteplase Hydrolases Circulatory system Hemodynamics Fibrinolytic |
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| Snippet | The renal medulla is a major source of plasminogen activators (PA), recently shown to induce vasodilation in vitro. Treatment with PA inhibitors has been... 1. The renal medulla is a major source of plasminogen activators (PA), recently shown to induce vasodilation in vitro. Treatment with PA inhibitors has been... The renal medulla is a major source of plasminogen activators (PA), recently shown to induce vasodilation in vitro . Treatment with PA inhibitors has been... |
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| SubjectTerms | aminocaproic acid Aminocaproic Acid - pharmacology Animals Aorta Biological and medical sciences calcium Calcium - metabolism Cells, Cultured Fibrinolytic Agents - pharmacology Hemodynamics Humans In Vitro Techniques Isometric Contraction - drug effects Kidney Kidney Medulla - blood supply Kidney Medulla - drug effects laser Doppler Medical sciences medulla microcirculation Microcirculation - drug effects Muscle, Smooth, Vascular - physiology Perfusion Pharmacology. Drug treatments Plasminogen Inactivators - pharmacology rat Rats Rats, Sprague-Dawley Renal Circulation - drug effects reteplase tissue plasminogen activator Tissue Plasminogen Activator - pharmacology vascular smooth muscle Vasoconstriction - drug effects |
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| Title | The fibrinolytic system attenuates vascular tone: effects of tissue plasminogen activator (tPA) and aminocaproic acid on renal microcirculation |
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