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First published online June 15, 2006
Journal of Experimental Biology 209, 2586-2594 (2006)
Published by The Company of Biologists 2006
doi: 10.1242/jeb.02290
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Effect of pH on trout blood vessels and gill vascular resistance

Michael P. Smith, Ryan A. Dombkowski, Jeffrey T. Wincko and Kenneth R. Olson*

Indiana University School of Medicine-South Bend Center, 1234 Notre Dame Avenue, South Bend, IN 46617, USA and Department of Biological Sciences, University of Notre Dame, Notre Dame, IN 46556, USA


Figure 1
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  		Fig. 1. Effects of extracellular pH (pHo) on tension of unstimulated efferent branchial arteries (EBA; N=11) and anterior cardinal veins (ACV; N=11) in Hepes buffer, and on vascular resistance of rainbow trout gills (11 gills from four trout) perfused with phosphate-buffered saline. Values are means ± s.e.m. EBA and ACV values are significantly different from their respective control (pH 7.8) except at pH 7.4; all vascular resistances except at pH 7.4 and 7.0 are significantly different from that at pH 7.8.

 

Figure 2
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  		Fig. 2. Effects of extracellular pH on efferent branchial artery contractions produced by arginine vasotocin (AVT; 1 nmol l–1), potassium chloride (KCl; 50 mmol l–1) or potassium acetate (KAc; 50 mmol l–1) in phosphate (PBS) or Hepes buffer. Values are means ± s.e.m. (N=4). *Different from same agonist (KCl or KAc) at all pH values lower than 8.2 or 8.6; {dagger}different from AVT at higher pH.

 

Figure 3
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  		Fig. 3. Effects of changing extracellular pH on tension produced during continuous exposure of efferent branchial arteries to arginine vasotocin (AVT; 1 nmol l–1) or KCl (50 mmol l–1) in Hepes buffer. (A) Raising pH from 7.4 to 8.2 did not significantly affect contraction, whereas AVT and KCl contractions were significantly ({dagger}) decreased when pH was lowered from 8.2 to 7.4. (B) Representative tracings of the KCl responses. Values are means ± s.e.m. (N=4).

 

Figure 4
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  		Fig. 4. Representative traces showing the effects of changing intracellular pH on resting tension of afferent (ABA) and efferent (EBA) branchial and celiacomesenteric (CMA) arteries in Hepes and Cortland buffer. Application of 40 mmol l–1 NH4Cl produces intracellular alkalosis and its removal produces acidosis. Vertical scale bar = 1 g tension in all traces.

 

Figure 5
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  		Fig. 5. Effects of buffer composition on the response of efferent branchial arteries to addition of 40 mmol l–1 NH4Cl (intracellular alkalosis) and NH4Cl washout (Wash; intracellular acidosis) 30 min later. Addition of 10 mmol l–1 NaHCO3 to Hepes (Hepes +HCO3–) did not affect the contraction accompanying NH4Cl addition or washout, whereas in Cortland buffer, addition of NH4Cl produced a significant relaxation ({dagger}) and washout produced a contraction that was significantly greater than the corresponding contraction in either Hepes or Hepes + HCO3– (*). Values are means ± s.e.m.; Hepes (N=14), Hepes+HCO–3 (N=4), Cortland (N=8).

 

Figure 6
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  		Fig. 6. Representative traces showing the effects of intracellular alkalosis (addition of 40 mmol l–1 NH4Cl) and acidosis (removal of NH4Cl) on tension of KCl (50 mmol l–1)- and U-46619-contracted efferent branchial arteries in Hepes buffer. Two NH4Cl exposures, 10 and 30+ min, are shown. Intracellular alkalosis contracts, and acidosis relaxes, KCl-stimulated vessels; these responses are reversed when the vessels are pre-contracted with U-46619. Vertical scale bars = 1 g.

 

Figure 7
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  		Fig. 7. Effects of buffer composition on the response of KCl (40 mmol l–1) pre-contracted efferent branchial arteries to addition of 40 mmol l–1 NH4Cl and NH4Cl washout (Wash) 30 min later. Buffer composition did not affect the KCl contraction nor the contraction accompanying NH4Cl addition. *The contraction accompanying NH4Cl washout was significantly weaker in Cortland than in Hepes buffer. Values are means ± s.e.m.; Hepes (N=4), Cortland (N=4).

 

Figure 8
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  		Fig. 8. Effects of buffer composition on the response of U-46619 (1 µmol l–1) pre-contracted efferent branchial arteries to addition of 40 mmol l–1 NH4Cl and NH4Cl washout (Wash) 30 min later. Only alkalosis was affected by buffer composition. Values are means ± s.e.m.; Hepes (N=6), Cortland (N=4). *Significantly different from each other.

 

Figure 9
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  		Fig. 9. Effect of L-type calcium channel inhibition (D600= methoxyverapamil; 0.1 mmol l–1) and zero extracellular calcium (0[Ca2+]o) on response of efferent branchial arteries to intracellular alkalosis (NH4Cl addition) and acidosis (NH4Cl washout) in Hepes buffer. Values expressed as percentage of an 80 mmol l–1 KCl contraction. *Significantly different from control. Values are means ± s.e.m.; Control (N=14), D600 (N=10), 0[Ca2+]o (N=8).

 

Figure 10
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  		Fig. 10. Role of L-type calcium channels and extracellular calcium on 40 mmol l–1 KCl contractions and on intracellular alkalosis and acidosis (NH4Cl and wash, respectively) in KCl pre-contracted efferent branchial arteries in Hepes buffer. *Significantly different from respective control. All values (means ± s.e.m.) expressed as a percentage of an 80 mmol l–1 KCl contraction.

 

Figure 11
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  		Fig. 11. Role of L-type calcium channels and extracellular calcium on U-46619 contractions (U-46 peak and U-46 plateau) and on intracellular alkalosis and acidosis (NH4Cl and wash, respectively) in U-46619 pre-contracted efferent branchial arteries in Hepes buffer. *Significantly different from respective control. All values (means ± s.e.m.) expressed as a percentage of an 80 mmol l–1 KCl contraction. Control (N=6), D600 (N=4), 0[Ca2+]o (N=4).

 

Figure 12
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  		Fig. 12. Effectiveness and reproducibility of acidity-induced reductions in gill resistance in isolated perfused gills of rainbow trout. Values are means ± s.e.m.; N=9 gills from five trout. *Significantly different from initial resistance at pH 7.8.

 




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