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N C Turner

Publications and source records attributed to N C Turner.

At least 37 records · Page 2Linked to original sources
PubMed1994

Relaxation of guinea-pig trachea by cyclic AMP phosphodiesterase inhibitors and their enhancement by sodium nitroprusside.

1. The effects of agents that elevate either cyclic AMP (the phosphodiesterase (PDE) III inhibitor siguazodan, salbutamol) or cyclic GMP (sodium nitroprusside (SNP)) on the relaxant activity of the PDE IV inhibitor, rolipram, were investigated in carbachol (0.1 microM) precontracted guinea-pig tracheal sheets. 2. Rolipram, siguazodan and SNP caused concentration-related reductions in tone of tissues precontracted with 0.1 microM carbachol (EC50 values 12.5; 2.73 and 0.35 microM respectively). Whilst the concentration-response relationship for the PDE III inhibitor, siguazodan, was monophasic that of the PDE IV inhibitor, rolipram, was biphasic. 3. The relaxant activity of rolipram was markedly enhanced in the presence of 10 microM siguazodan (EC50 < 0.01 microM), 0.1 microM salbutamol (EC50 0.03 microM) and 0.3 microM SNP (EC50 0.03 microM). In contrast, the relaxant activity of siguazodan was unaffected by SNP and only modestly enhanced by rolipram (10 microM) and salbutamol (0.1 microM). 4. The relaxant activity of SNP was enhanced by the PDE V inhibitor SK&F 96231 (30 microM: EC50 0.06 microM) and rolipram (30 microM, EC50 0.08 microM) but was unaffected by 30 microM siguazodan. 5. At concentrations up to 10 microM, neither siguazodan nor rolipram elevated tracheal cyclic AMP levels. However, the combination of 10 microM rolipram and siguazodan caused a two fold increase in the cyclic AMP content (from 2.19 to 4.36 pmol cyclic AMP mg-1 protein). SNP (0.1-10 microM) failed to produce a significant increase in tracheal cyclic AMP levels. At 0.1 microM the effect of SNP on tracheal cyclic AMP levels was significantly (P < 0.05) increased in the presence of rolipram but not siguadozan. 6. The results indicate that the relaxant effects of rolipram are markedly enhanced by agents that inhibit PDE III activity or elevate cyclic GMP. They support the hypothesis that SNP potentiates the effects of rolipram via the inhibitory action of cyclic GMP on hydrolysis of cyclic AMP by PDE III. The findings also suggest that whilst PDE III may be more significant in regulating basal smooth muscle tone in the absence of any exogenous stimulus to cyclic AMP accumulation, PDE IV activity may be more tightly coupled to the pool of adenylyl cyclase stimulated by beta2-adrenoceptor agonists.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1994

Pulmonary effects of type V cyclic GMP specific phosphodiesterase inhibition in the anaesthetized guinea-pig.

1. We have investigated the bronchodilator potential of type V phosphodiesterase (PDE V) inhibitors in anaesthetized ventilated guinea-pigs using the potent and selective PDE V inhibitor, SK&F 96231. We have compared its activity to that of salbutamol, the PDE III inhibitors, siguazodan and SK&F 95654 and to the PDE IV inhibitor rolipram. 2. Administered as an i.v. infusion SK&F 96231 (0.6 and 1 mg kg-1 min-1, i.v.) caused a slowly developing inhibition of histamine (100 nmol kg-1, i.v.)-induced bronchoconstriction and elevated tracheal cyclic GMP levels in the anaesthetized guinea-pig. SK&F 96231 (0.1 and 0.3 mg kg-1 min-1, i.v.) was without effect on histamine-induced bronchoconstriction. In the presence of a sub-threshold infusion of SNP (0.1 mumol kg-1 min-1, i.v.) there was a marked enhancement of SK&F 96231-induced inhibition of histamine responses such that at infusion rates that were ineffective alone, SK&F 96231 caused a > 50% inhibition of histamine responses. The stimulation of tracheal cyclic GMP accumulation by SK&F 96231 was also potentiated. 3. Administered directly into the airway, SK&F 96231 (300 micrograms in 5 mg lactose carrier) was largely without effect on histamine-induced bronchoconstriction (4.9 +/- 1.9% inhibition). In the presence of SNP (0.1 mumol kg-1 min-1, i.v.) or isosorbide dinitrate (200 micrograms administered by insufflation into the trachea) there was a marked potentiation of the inhibitory activity of SK&F 96231 (40 +/- 4% and 62 +/- 1.8% respectively). 4. Salbutamol and rolipram (3-300 microg by insufflation) caused a dose-related inhibition of histamine responses with a maximum of 91 +/- 2% and 59 +/- 10% respectively. The PDE III inhibitor, siguazodan,was without effect on histamine responses but they were reduced (27.7 +/- 4.8% at 300 microg) by SK&F95654. There was a marked enhancement of the inhibitory activity of rolipram in the presence of SK&F 95654.5. We conclude that SK&F 96231 has weak anti-spasmogenic activity in the guinea-pig in vivo, we suggest that this is primarily a consequence of a low endogenous guanylate cyclase activity in the airway. The potentiation of the anti-spasmogenic activity of SK&F 96231 by SNP suggests that a combination of PDE V inhibitor and guanylate cyclase agonist might provide significant bronchodilator activity.6. We have established that PDE IV inhibitors are bronchodilators when administered directly into the airway of anaesthetized guinea-pigs but that PDE III inhibitors are only weakly active. The marked enhancement of the inhibitory activity of rolipram by the PDE III inhibitor, SK&F 95654, indicates that inhibitors of both PDE III and PDE IV might offer greater potential as bronchodilators than inhibitors of either isoenzyme alone.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1994

Effects of PAF, FMLP and opsonized zymosan on the release of ECP, elastase and superoxide from human granulocytes.

Platelet-activating factor (PAF) is a potent chemoattractant for human eosinophils and neutrophils and causes eosinophil and neutrophil recruitment into animal airways. Since eosinophils and eosinophil cationic proteins are thought to play an important role in the pathophysiology of asthma, we have examined the hypothesis that PAF may also stimulate eosinophil cationic protein (ECP) release from human granulocytes. Granulocytes (93% neutrophils, 3% eosinophils) were isolated from the blood of normal volunteers, using metrizamide density gradients, and stimulated in vitro with PAF, L-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP) or opsonized zymosan (OPZ). Superoxide generation was measured colorimetrically, granulocyte degranulation by a fluorimetric assay for elastase, and eosinophil activation by specific radioimmunoassay (RIA) for ECP. Granulocyte chemotaxis was also measured. Whilst both PAF and FMLP were potent chemoattractants for human mixed granulocytes (concentrations producing half the maximal effect (EC50s) ca 10 nM), PAF at concentrations below 10 microM was a poor stimulus to superoxide generation, elastase release or ECP release from the same cell population. In contrast, FMLP was a potent stimulus to both superoxide generation (EC50 48 nM) and ECP (EC50 ca 100 nM) and elastase release (EC50 ca 1 microM). OPZ was a potent stimulus to superoxide generation, but was a poor stimulus to ECP or elastase release. Thus, although PAF is a potent chemoattractant for human granulocytes, our results suggest that it alone may not stimulate their subsequent activation and release of cytotoxic products.

Blood Proteins↗
PubMed1993

The effect of cyclic AMP and cyclic GMP phosphodiesterase inhibitors on the superoxide burst of guinea-pig peritoneal macrophages.

1. The cyclic nucleotide phosphodiesterase (PDE) activity of guinea-pig peritoneal macrophages was partially characterized and the effects of selective and non-selective inhibitors of adenosine 3':5'-cyclic monophosphate (cyclic AMP PDE) and guanosine 3':5'-cyclic monophosphate (cyclic GMP PDE) phosphodiesterases on superoxide generation were investigated using peritoneal macrophages from horse-serum pretreated guinea-pigs. 2. The non-selective PDE inhibitor, 3-isobutyl-1-methylxanthine (IBMX) and the PDE I/V selective inhibitor, zaprinast, inhibited spontaneous superoxide generation with IC50s of 30.7 +/- 11.3 microM and 145 +/- 17 microM respectively (n = 6 and 5). The concentration-response curves for the PDE IV selective inhibitors rolipram and Ro20-1724 were biphasic; mean maximum inhibitions were 56.9 +/- 5.9% and 66.8 +/- 10.5% respectively at 300 microM, but in 2 out of 6 (rolipram) and 2 out of 5 (Ro20-1724) experiments inhibition was < 50%. The PDE III inhibitor SK&F 94120 was without effect. Spontaneous superoxide generation was reduced 57 +/- 10% by 1 microM prostaglandin E2 (PGE2) and 62.6 +/- 3.76% by 1 microM salbutamol. 3. The increase in superoxide generation elicited by FMLP (10(-9)-10(-5)M) was unaffected by any of the PDE inhibitors studied. Inhibition of FMLP-stimulated superoxide generation by PGE2 was enhanced in the presence of 10 microM IBMX. 4. Macrophages were found to contain a predominantly membrane bound cyclic AMP PDE (90% of total activity) which was unaffected by cyclic GMP or calcium/calmodulin. The cyclic AMP PDE activity in the cytosolic fraction was enhanced in the presence of calcium/calmodulin. Selective inhibitors of PDE IV inhibited the particulate cyclic AMP PDE activity (IC50s rolipram 1.5 +/- 0.3 microM, Ro 20-17244.1 +/- 0.6 microm) as did the non-selective inhibitor IBMX (IC50 22 +/- 8 microM). The macrophage particulate PDE activity was resistant to inhibition by the PDE III inhibitor SK&F 94836 and the PDE I/V inhibitor, zaprinast. The cytosolic calcium/calmodulin stimulated cyclic AMP hydrolytic activity was inhibited by zaprinast (IC50 - calcium/calmodulin 123 +/- 39 microM; + calcium/calmodulin IC50 17.7 +/- 6.3 microM).5. The results indicate that guinea-pig peritoneal macrophages contain a type IV cyclic AMP PDE which is predominantly membrane associated and a predominantly cytosolic calcium/calmodulin stimulated cyclic AMP PDE. Functional studies suggest that both of these PDE activities contribute to cyclic AMP hydrolysis and regulation of superoxide generation in these cells. Inhibition of spontaneous superoxide generation, but not that stimulated by FMLP, suggests that the activity of PDE inhibitors is subject to functional antagonism but that this can be overcome by enhancing cyclic AMP formation.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1992

Characterization of the antagonist activity of the PAF antagonists RP 59227 and WEB 2086 on elicited guinea pig peritoneal macrophages. Evidence for variable affinities and kinetics.

The pharmacological selectivity and affinity of the two PAF antagonists RP 59227 and WEB 2086 for macrophage platelet activating factor (PAF) receptors have been investigated. PAF produced a dose-related increase in superoxide generation from elicited guinea pig peritoneal macrophages (IC50 41 +/- 16 nM, n = 9). After a 5 min preincubation time RP 59227 (0.1, 1.0 and 10 microM) produced a dose-related rightward displacement of the PAF dose-response curve, the Schild plot gave a pA2 of 7.39 +/- 0.07 (n = 5) with a slope of 1.17 +/- 0.11, indicating competitive antagonism. WEB 2086 over the same concentration range was without effect at the lower two concentrations, but at 10 microM, the displacement of the PAF dose-response curve was similar to that obtained with 10 microM RP 59227. Increasing the preincubation time to 30 min increased the affinity of RP 59227 (apparent pA2 8.76 +/- 0.28, n = 5). This was associated with a reduction in the slope of the Schild plot to 0.67 +/- 0.11, suggesting noncompetitive kinetics. The affinity of WEB 2086 could not be determined, but the antagonism appeared noncompetitive in nature. The results indicate that PAF antagonists can show variable affinities for macrophage PAF receptors depending on the experimental conditions, as well as competitive or noncompetitive kinetics depending on the contact time.

Animals↗
PubMed1991

Characterization of guinea-pig eosinophil phosphodiesterase activity. Assessment of its involvement in regulating superoxide generation.

Experiments have been performed to characterize guinea-pig peritoneal eosinophil cyclic nucleotide phosphodiesterase (PDE) activity and establish whether it is involved in regulating superoxide (.O2-) generation. Eosinophils were found to contain a predominantly membrane-bound cAMP PDE(s) (92.5 +/- 2.4% of total activity) which was resistant to solubilization with Triton X-100 (1%). This particulate PDE exhibited complex kinetics (Km = 1.3 and 31.4 microM) and was unaffected by cGMP (IC50 greater than 100 microM) or CaCl2 (2 mM) + calmodulin (10 units/mL). Little cGMP PDE activity was detected in either the soluble or particulate fractions. Inhibitors of the Ro-20-1724-inhibited (Type IV) cAMP PDE, namely Ro-20-1724 (IC50 = 0.92 +/- 0.43 microM), rolipram (IC50 = 0.20 +/- 0.04 microM) and denbufylline (IC50 = 0.20 +/- 0.01 microM), potently inhibited the particulate cAMP PDE, as did the non-selective inhibitors trequinsin (IC50 = 0.11 +/- 0.02 microM) and AH-21-132 (IC50 = 2.57 +/- 0.02 microM). Eosinophil cAMP PDE was resistant to SK&F 94120 (IC50 greater than 1000 microM), the cGMP-inhibited (Type III) cAMP PDE inhibitor, and the cGMP PDE (Type I) inhibitor, zaprinast, was only weakly active (IC50 = 35.33 +/- 10.74 microM). .O2- release from resting cells was potently inhibited by rolipram (IC50 = 0.05 +/- 0.03 microM) and denbufylline (IC50 = 0.06 +/- 0.04 microM) but surprisingly, in view of its potent cAMP PDE inhibitory activity, was only weakly decreased by trequinsin (IC50 = 8.0 +/- 2.7 microM). AH-21-132 (IC50 greater than 10 microM), SK&F 94120 (IC50 greater than 10 microM) and zaprinast (IC50 greater than 10 microM) were without effect. Rolipram and denbufylline alone exerted little effect on cAMP in intact cells but, in the presence of 10 microM isoprenaline, potently increased intracellular accumulation (EC50 = 0.45 +/- 0.16 and 0.28 +/- 0.08 microM, respectively). Trequinsin and AH-21-132 only weakly enhanced isoprenaline-stimulated cAMP accumulation. Although it induced a marked rise in cAMP only in the presence of isoprenaline, rolipram (50 microM) alone was able to increase the activity ratio of cAMP-dependent protein kinase from 0.24 to 0.84. The results suggest that Ro-20-1724-inhibited cAMP PDE plays a role in regulating eosinophil .O2- generation. The poor correlation between the PDE inhibitory actions of certain compounds and their effectiveness in elevating cAMP and inhibiting .O2- suggests the existence of a barrier impeding access to the enzyme.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1990

Effects of nonsteroidal anti-inflammatory drugs on the bronchial hyperresponsiveness of middle-aged male smokers.

Bronchial hyperresponsiveness (BHR) in smokers is believed to be a consequence of airway wall inflammation. We have examined the effects of treatment with nonsteroidal anti-inflammatory drugs (NSAID) on BHR to inhaled histamine, measured as the provocative concentration reducing forced expiratory volume in one second (FEV1) by 20% (PC20), in middle-aged male cigarette smokers in two separate double-blind, placebo-controlled, cross-over trials. Baseline FEV1 in these smokers ranged from 41-117% predicted values. In the first study 15 men (mean age 58 yrs, FEV1 2.20 l) were examined before and one hour after a single dose of 1.2 g aspirin. There was no significant change in PC20 (geometric mean 1.88 mg.ml-1 pre-aspirin, 1.89 mg.ml-1 post-aspirin) or baseline FEV1 and we observed no tachyphylaxis to the effects of inhaled histamine at one hour after placebo. In the second study 10 men (mean age 60 yrs, FEV1 2.53 l) were examined before and after three days' treatment with the NSAID flurbiprofen 50 mg t.d.s. Baseline PC20 was higher in this group than in the first study. There was no relationship between the excretion of urinary thromboxane metabolites and the intensity of BHR under baseline conditions; flurbiprofen greatly reduced the urinary excretion of thromboxane metabolites, but baseline FEV1 was not altered. Analysis of change in PC20 was complicated by a difference in baseline PC20 before the two treatments, but treatment with flurbiprofen did not significantly attenuate BHR. The results suggest that thromboxane or other cyclo-oxygenase products of arachidonic acid metabolism do not play an important role in the short-term maintenance of BHR to histamine in middle-aged male cigarette smokers.

Aged↗
PubMed1989

Endothelin-1-induced contractions of vascular and tracheal smooth muscle: effects of nicardipine and BRL 34915.

Endothelin-1 (ET-1) produced concentration-dependent contractions of rat aorta and rat trachea. These contractions were dependent on the presence of extracellular calcium but unaffected by nicardipine. Contractions of aorta could be attenuated with the potassium channel activator BRL 34915. BRL 34915 also elicited dose-related relaxations of rat aorta and trachea precontracted with ET-1. We conclude that although the increase in calcium permeability elicited by ET-1 may not involve dihydropyridine-sensitive calcium channels, its reversal by BRL 34915 suggests that smooth muscle contraction by ET-1 may involve a voltage-linked mechanism.

Animals↗
PubMed1989

Endothelin-induced contractions of tracheal smooth muscle and identification of specific endothelin binding sites in the trachea of the rat.

1. The presence of specific binding sites and the contractile activity of the novel peptide, endothelin have been investigated in rat trachea. 2. Endothelin (10(-8)-10(-5) M) induced long-lasting contraction of rat tracheal rings superfused with Krebs solution (EC50 5.4 x 10(-6) M). Contractions of the tissue to 10(-6) M endothelin were attenuated in Ca2+-free medium containing 0.1 mM EGTA but unaffected by nicardipine (10(-7) M). 3. After equilibration in Ca2+-free medium (without EGTA) a return to normal Ca2+ concentrations (2.5 mM), 30 min or 60 min following endothelin (10(-6) M), produced a sustained contraction of the tissue. 4. Specific binding sites for endothelin were identified on rat tracheal smooth muscle (KD 1.34 x 10(-10) M, maximal binding 1.2 fmol mm-2). Specific binding sites were also identified on nerve trunks. Endothelin binding was unaffected by co-incubation with nicardipine (10(-7) M) or verapamil (10(-7) M). 5. The discrepancy between the apparent KD for endothelin binding and the EC50 for endothelin-induced contraction suggests that the endothelin binding sites identified in this study may not be associated with the receptors mediating contraction. 6. These results indicate that endothelin binding sites are present on tracheal smooth muscle. The mechanism of endothelin-induced contraction, whilst being dependent on extracellular calcium, does not appear to involve binding to the dihydropyridine- or verapamil-sensitive sites on the voltage-dependent Ca2+ channel. Its long duration of action may be associated with a sustained increase in Ca2+ permeability.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1989

Oral N-acetylcysteine or S-carboxymethylcysteine inhibit cigarette smoke-induced hypersecretion of mucus in rat larynx and trachea in situ.

Two weeks exposure of rats to cigarette smoke (CS) significantly (p less than 0.05) increased the secretion of fucose-containing glycoconjugates above normal in an in situ preparation of larynx and trachea. After equilibration mean basal secretion in CS-exposed rats was 24 micrograms (per 30 min collection) which was 8 times higher than that of unexposed animals (p less than 0.01). N-acetylcysteine (NAC) or S-carboxymethylcysteine (SCMC) given as 1% of the drinking water, before and after daily exposure to CS, significantly inhibited the development of the CS-induced increase in fucose secretion reducing the mean for basal secretion in each group to 7 and 5 micrograms, respectively (p less than 0.05). Neither NAC nor SCMC had significant effects on baseline glycoconjugate secretion in control animals. Albumin was inconsistently present in the secretions of both control and CS-exposed animals, whereas in those exposed to CS and also given one of the two cysteine derivatives there was a consistent increase in albumin transudation.

Acetylcysteine↗
PubMed1988

Release of arachidonic acid metabolites and histamine from sensitized guinea-pig lung following antigen challenge.

1. The time course of mediator release and the hypothesis that the ratio of eicosanoids to histamine might alter with the intensity of stimulus or its route of administration has been explored in isolated perfused lung from sensitized guinea-pigs challenged with ovalbumin. 2. Histamine and prostaglandin release was rapid in onset and virtually complete within 10 min. Thromboxane B2 (TXB2) and leukotriene D4 (LTD4) release, however, was more sustained. Release of the major prostanoid metabolites was relatively delayed compared to that of the parent compounds and was more sustained. 3. Mediator release was antigen-dose dependent and TXB2, prostaglandin D2 (PGD2) and LTD4 release linearly related to histamine concentrations (P less than 0.05). However, the ratio of the percentage maximum release of eicosanoids relative to histamine was greatest with low doses of ovalbumin. 4. At a low antigen dose (10 micrograms ovalbumin), histamine and prostanoid release was greatest when the challenge was via the airway rather than into the pulmonary artery and the greatest differences were in PGF2 alpha levels. At near maximal challenge (1 mg ovalbumin) there was little difference in concentrations of PGD2, TXB2, 6-oxo-PGF1 alpha and LTD4 by either route, but PGF2 alpha levels remained greater. 5. The results indicate that biologically active amounts of prostanoids may be released from sensitized lung at low degrees of mast cell activation and that differences in mediator release following antigen administration to the airway or into the pulmonary vasculature simply reflects its accessibility to sensitized cells.

Animals↗
PubMed1987

Single-step procedure for the extraction and purification of leukotrienes B4, C4 and D4.

A rapid and simple method for the on-line concentration and high-performance liquid chromatographic (HPLC) purification of the leukotrienes in good yield from biological fluids is described. Readily available antisera are used in conjunction with this system to give a specific and sensitive assay for leukotrienes B4, C4 and D4 with sub-nanogram limits of detection. Tritium-labelled leukotrienes are used as internal standards, both to locate the leukotrienes post-HPLC and to accurately determine recoveries.

Animals↗
PubMed1987

Cigarette smoke-induced 'chronic bronchitis': a study in situ of laryngo-tracheal hypersecretion in the rat.

Mucous secretion and mucosal permeability by the larynx and trachea, isolated in situ, was investigated in normal rats and in those in which 'chronic bronchitis' was induced by daily exposure to cigarette smoke for 2 weeks. Fucose was used as a specific marker for the secretion of mucus glycoprotein, and hexose and protein were markers both for mucus and plasma-type glycoproteins present in tissue fluid transudate. Albumin was used as an indicator of the contribution of serum to the secretions. After equilibration, the mean basal secretion of fucose (microgram/30 min collection) was significantly higher in 'bronchitic' rats than in the controls (P less than 0.01). Mean values for controls were: fucose 3 (SEM 1: n = 9), hexose 41 (SEM 9; n = 8), protein 1082 (SEM 385; n = 8), albumin less than 2 (n = 8); for 'bronchitic' rats the values were: 24 (SEM 6; n = 7), 101 (SEM 26; n = 8), 2000 (SEM 520; n = 8) and less than 2 micrograms (n = 7) respectively. In control and bronchitic animals acute administrations of cigarette smoke, blown directly through the laryngo-tracheal segment after equilibration, caused significant (P less than 0.05) transient increases in the secretion of fucose, hexose and protein, but not of albumin.

Animals↗
PubMed1985

The influence of native porcine gastric mucus gel on hydrogen ion diffusion: the effect of potentially ulcerogenic agents.

Experiments were carried out to investigate the ability of native gastric mucus gels to retard hydrogen ion diffusion. Mucus held between two polycarbonate membrane filters in a diffusion cell, separating equimolar solutions of NaCl and HCl, significantly reduced the rate of hydrogen ion diffusion and increased the time for the mean hydrogen ion front to traverse the mucus compartment (lag time) when compared to an unstirred layer of saline (P less than 0.01). N-acetylcysteine, sodium taurodeoxycholate and acetylsalicylic acid significantly increased the diffusion rate (P less than 0.025); the lag time was significantly reduced by N-acetylcysteine (P less than 0.001). In addition mucus gels were found to have buffering capacity at a pH greater than 2. These observations suggest that native gastric mucus gels can retard hydrogen ion diffusion and that this retardation of diffusion is reduced by agents which are potentially damaging to the gastric mucosa.

Animals↗
PubMed1984

Comparison of water potentials measured by in situ psychrometry and pressure chamber in morphologically different species.

Leaf water potentials measured by in situ psychrometry were compared with leaf water potentials measured by the pressure chamber technique at various values of water potential in Helianthus annuus, Helianthus nuttallii, Vigna unguiculata, Nerium oleander, Pistacia vera, and Corylus avellana. In V. unguiculata, the leaf water potentials measured by the in situ psychrometer oscillated at the same periodicity as, and proportional to, the leaf conductance. In all species, potentials measured by in situ psychrometers operating in the psychrometric mode were linearly correlated with potentials measured with the pressure chamber. However, the in situ psychrometers underestimated the leaf water potential in the two Helianthus species at low water potentials and overestimated the water potential in P. vera, N. oleander, and C. avellana. The underestimation in the two Helianthus species at low water potentials resulted from differences in water potential across the leaf. The overestimation in P. vera, N. oleander, and C. avellana was considered to arise from low epidermal conductances in these species even after abrasion of the cuticle. Pressure-volume studies with Lycopersicon esculentum showed that less water was expressed from distal than proximal leaflets when the whole leaf was slowly pressurized. The implication of this for water relations characteristics obtained by pressure-volume techniques is discussed. We conclude that in situ psychrometers are suitable for following dynamic changes in leaf water potential, but should be used with caution on leaves with low epidermal conductances.

Journal Article↗
PubMed1984

Influence of Osmotic Adjustment on Leaf Rolling and Tissue Death in Rice (Oryza sativa L.).

Osmotic adjustment, measured by the lowering of the osmotic potential at full turgor, and its influence on leaf rolling and leaf death was assessed in the lowland rice (Oryza sativa L.) cultivar IR36 in both the greenhouse and field. The degree of osmotic adjustment varied with the degree and duration of stress, but was usually 0.5 to 0.6 megapascal (maximally 0.8 to 0.9 megapascal) under severe stress conditions. In leaves in which osmotic adjustment was 0.5 to 0.6 megapascal, leaf rolling and leaf death occurred at lower leaf water potentials in adjusted than in nonadjusted leaves. We conclude that osmotic adjustment aids in the drought resistance of rice by delaying leaf rolling, thereby maintaining gas exchange, and by delaying leaf death.

Journal Article↗