Plasma Renin Activity Following Central Infusion of Angiotensin II and Altered CSF Sodium Concentration in the Conscious Goat

To study central influences on the renal release of renin, angiotensin II was infused into the lateral cerebral ventricle of conscious hydrated goats. CSF sodium concentration was increased or lowered by similar infusions of hypertonic NaCl or of isotonic fructose solution. Infusion of anglotensin II in doses from 0.5 to 1 μg caused a drop in plasma renin activity (PRA) and elicited a rise in blood pressure, antidiuresis, natriuresis, and thirst. Intraventricular infusion of hypertonic NaCl also suppressed PRA, induced anti-diuresis, natriuresis, and an inconsistent rise in blood pressure. Lowering of CSF [Na⁺] by infusion of isotonic fructose caused a rise in PRA and was followed by a water diuresis in the non-hydrated animal. The fructose infusions caused some decrease in renal K⁺ excretion but no consistent change in renal Na⁺ excretion. The results indicate that angiotensin II and changes in sodium balance modulate renal renin release also via the central nervous system.     

Canjoint Action of Sodium and Angiotensin on Brain Mechanisms Controlling Water and Salt Balances

Andersson , B. and L. Eriksson , Conjoint action of sodium and angiotensin on brain mechanisms controlling water and salt balances. Acta physiol. scand. 1971. 81. 18–29. The effects on water and salt balances of a simultaneous infusion of angiotensin and hypertonic NaCl into the 3rd brain ventricle were studied in goats in normal water balance and in hydrated animals. For comparison similar infusions of angiotensin alone (solved in slightly hypotonic saline) and of hypertonic NaCl were made. Like the hypertonic NaCl, 30 min infusions of angiotensin alone induced drinking in animals in normal water balance, and an inhibition of the water diuresis in the hydrated goat. The simultaneous infusion of both substances resulted in a marked potentiation of the dipsogenic and the antidiuretic effects. A possible explanation may be that angiotensin facilitates the transport of Na⁺ into brain cells regulating thirst and ADH release, and that the intracellular Na⁺ concentration rather than strictly osmotic factors determines the activity of these cells. In the hydrated goat a central effect of angiotensin strongly enhanced the natriuretic response to intraventricular infusions of hypertonic NaCl, and extreme natriuresis developed as result of the combined infusions in hydrated, salt-supplemented animals. During normal water balance this sodium-angiotensin synergism was less obvious, which suggests that both an expanded fluid volume and an elevated intracellular Na⁺ concentration are needed for optimal activation of a brain mechanism which stimulates renal Na' excretion, The time course of the centrally induced natriuresis indicates that the effect on the kidney may be mediated by a humoral agent.     

Transient vasopressin release and thirst in response to prolonged intracerebroventricular infusions of hypertonic mannitol in saline

In the conscious goat infusions of 0.4 M mannitol in 0.15 M NaCl into the lateral cerebral ventricle (40 or 100 min, 0.02 ml/min) caused slight, transient vasopressin release and temporary thirst, whereas infusions or pure, hypertonic (0.7 M) mannitol did not elicit thirst and inhibited the basic vasopressin release in the nonhydrated animal. In contrast, infusions of equiosmolal (0.35 M) NaCl induced persistent thirst and pronounced elevation of the plasma vasopressin concentration throughout the infusion period. The cerebrospinal fluid (CSF) osmolality was raised by the same order of magnitude (= 13%) after the mannitol/NaCl and the hypertonic NaCl infusions. The CSF Na+ concentration was elevated by greater than 10% at 5 min after hypertonic NaCl infusions, but it was reduced by approximately 10% at 5 min after the mannitol/NaCl infusions. There was no appreciable difference in the CSF K+ concentration after the infusions. The results are discussed with regard to the possible importance of CSF Na+-concentration as opposed to strict osmotic factors for the excitation of receptors involved in the control of water balance.     

Interaction of changes in the third ventricular CSF tonicity, central and systemic AVP concentrations and water intake

Arginine vasopressin (AVP) is assumed to be involved as a central transmitter or modulator in the control of autonomic functions including thirst. In conscious dogs AVP concentration in cerebrospinal fluid (CSF) from the anterior part of the third ventricle (A3V) was analysed before and after local elevation of CSF osmolality by intracerebroventricular (i.c.v.) infusion of 0.35 M NaCl and after i.c.v. AVP infusion at 46 and 138 fmol ml-1 for 10 min. In addition, the effects of these i.c.v. infusions on water intake, plasma AVP concentration and blood pressure were investigated. In euhydrated dogs 0.35 M NaCl i.c.v. did not alter AVP concentration in the CSF during the subsequent 2 h. In contrast, plasma AVP concentration had increased significantly from 3.4 +/- 0.3 (control) to 6.4 +/- 0.7 and 4.7 +/- 0.3 fmol ml-1, 4 and 16 min, respectively, after the hypertonic stimulus. Drinking was stimulated with an average water intake of 14.5 +/- 3.7 ml kg-1 body wt. However, AVP infusion into the A3V did not elicit water intake despite increases of AVP concentration in the A3V by factors up to 40 above control. The same animals responded with spontaneous drinking to 0.35 M NaCl i.c.v. administered 160 min after the end of AVP infusions. Exogenously administered AVP disappeared from the A3V with a time constant of 13.8 min. The results do not support the view that AVP in the A3V CSF per se stimulates drinking.     

Duration of Central Action of Angiotensin II Estimated by its Interaction with CSF Na+

In pre-hydrated goats, an urge to drink persisted for approximately half an hour after combined infusions of angiotensin II and hypertonic (0.5 M) NaCl into the lateral or third cerebral ventricle. The intraventricular infusion of angiotensin/glucose solution, having no dipsogenic action of its own, markedly accentuated the dipsogenic and antidiuretic effects of the subsequent intraventricular infusion of hypertonic NaCl. The possibility is discussed that angiotensin may be bound at periventricular receptor sites where it continues to interact with Na⁺ in eliciting thirst and ADH release for about half an hour.     

Hypertension and thirst outlasting renal vasoconstriction as effects of a brief elevation of systemic angiotensin II in sheep

The influence of 10 min intracarotid (i.e.) and intravenous (i.v.) infusions of angiotensin II (Ang II; 20 pmol kg^-1 min^-1) on carotid blood pressure (cBP) and renal blood flow (RBF) was studied in unanaesthetized ewes without and with pre-treatment with the α₁-and β-adrenoceptor blocker labetalol. RBF was also monitored during 30 min intracerebroventricular (ICV) infusions of Ang II at 2 pmol kg^-1 min^-1. The i.e. infusions of Ang II induced about 50 mmHg rise in cBP. A steep decline occurred during 5 min post-infusion, followed by a much slower reduction with the cBP remaining above control level at 40 min post-infusion. The pressure elevation induced by i.v. Ang II was less pronounced but exhibited a similar pattern. Labetalol significantly reduced the pressor response to i.e. as well as i.v. Ang II. The i.e. and i.v. infusions of Ang II conspicuously reduced the RBF regardless of whether the ewes were labetalol-treated or not. At 5 min after the infusions RBF had returned to control level. The ICV infusions did not influence the RBF. Ang II i.e. elicited thirst in 50% of the ewes with the urge to drink remaining at 40 min post-infusion. The dipsogenic response was not reduced by labetalol pre-treatment. The results imply that no cerebral component contributes to the reduction in RBF induced by systemic Ang II. However, a centrally mediated action seems to be the cause of the long-lasting post-infusion cBP elevation and dipsogenic response. It suggests that, once bound at brain sites, Ang II may have a sustained action, alternatively may initiate cerebral processes of long duration.     

Influence of Prostaglandin E1 on Cerebral Mechanisms Involved in the Control of Fluid Balance

The effects of infusions of PGE₁ (30 ng/kg min^-1) into the lateral cerebral ventricle were studied in the conscious, hydrated goat. The infusions caused release of antidiuretic hormone and increased renal sodium excretion. When PGE₁ was infused together with hypertonic NaCl these effects became markedly enhanced and the infusion also induced drinking and a rise in the arterial blood pressure. Much weaker effects were obtained by the infusion of the hypertonic NaCl alone. This sodium-PGE₁ interaction is discussed in relation to previously observed, central sodium-angiotensin II interaction. A more pronounced drinking effect was obtained in response to the intraventricular infusion of PGE₁+ angiotensin II, than to the infusion of either substance separately. The PGE₁ administered into the lateral cerebral ventricle did not induce any febrile response.     

Effects on fluid balance induced by non-febrile intracerebroventricular infusions of PGE2, PGFZ2β, and arachidonic acid in the goat

Prostaglandins (PG) E₂, F_2α (30 ng/kg.min-¹) and arachidonic acid (150 and 300 ng/kg.min^-1) were infused for 30 min into the lateral cerebral ventricle of conscious hydrated and non-hydrated goats. Like previously shown as concerns PGE₁. PGE₂ was found to inhibit the water diuresis and cause some increase in the renal sodium excretion in the hydrated animal, and to elicit thirst in the non-hydrated goat. The effects of PGE₂ were enhanced when hypertonic (0.25 M) NaCl was simultaneously infused into the ventricle. The antidiuretic effect of PGF_2α, was less pronounced, and drinking only occasionally occurred when this PG was infused into the non-hydrated animal. Only a weak, post-infusion reduction of the water diuresis was observed when arachidonic acid was administered into the hydrated goat. Neither the PG:s, nor arachidonic acid affected the temperature regutation of the animals. The possibility is discussed that the lack of febrile response was due to the choice of platinum-iridium as material for the cerebral irnplantations. It is suggested that PGE, might have interacted with CSF Na⁺ in stimulating juxtaventricular receptors involved in the control of fluid balance. The experiments do not support the concept that PG:s of the E series constitute a cerebral humoral link in pyrogen-induced fever.     

Deuterium Induced Extinction of ADH-release in Response to Intracerebroventricular Infusions of Hypertonic NaCl and Angiotensin

Infusions (20μl/min) of hypertonic (0.3 M) NaCl and angiotensin 11 (1 ng/kg min^-1)in isotonic (0.15 M) NaCl were made for 1 h in the hydrated goat during fully developed water diuresis. Either H₂O or deuterium (D₂O) was used as solvent. A pronounced antidiuretic response, outlasting the infusion period by 30 min or more, was seen when the substances were dissolved in H₂O. Only a weak inhibition of the water diuresis, which was extinguished during the infusion period, was obtained when D₂O was used as the solvent. The infusion of 0.3 M NaCl/H₂O invariably induced drinking in one of the goats, which, however, showed no drinking response to the infusions of 0.3 M NaCl/D₂O. The possibility is discussed that D₂O (perhaps by-its inhibitory effect on (Na+-K+)-ATPase activity) reduced the sensitivity of juxtaventricular receptors regulating ADH-release and water intake.     

Spike conduction properties of T-shaped C neurons in the rabbit nodose ganglion

Noradrenaline (NA) and angiotensin II (A II) were infused intravenously in conscious dogs without (series I) and with (series II) additional infusions of sodium nitroprusside at doses re-establishing normal levels of mean arterial pressure (MAP). In series I, NA infusion (1.6 g/min per kg for 30 min) initially elevated MAP by some 25 mm Hg and lowered heart rate by some 30 beats/min. Plasma concentrations of arginine vasopressin (AVP) remained constant, while those of A II and atrial natriuretic factor were slightly, but significantly, increased. Infusion of A II (10 or 20 ng/min per kg for 30 min) induced similar rises in MAP and slight reductions of heart rate and increased plasma AVP by 70% and atrial natriuretic factor by 60%. In series II, sodium nitroprusside (1–4 g/min per kg) was added for 30 min to infusions of NE (1.6 g/min per kg) and A II (20 ng/min per kg) in order to maintain MAP at its control level. This resulted in an 11-fold increase in plasma AVP during NA infusion and a 19-fold increase during A II infusion. Infusing sodium nitroprusside (4 g/min per kg) alone lowered MAP to clearly hypotensive levels, but the resulting rises in plasma AVP were less than, rather than equal to, those seen at normotensive MAP levels during the combined infusions of sodium nitroprusside with A II or NA, respectively. It is concluded that both NA and A II exert strong stimulatory actions on AVP release which are, however, counteracted by inhibitory influences arising from the hypertensive effects of NA and A II.     

INCOMPATIBILITY FOR OR PRE-IMMUNIZATION AGAINST M1s DETERMINANTS DECREASES LETHAL GRAFT-VERSUS-HOST REACTION DEVELOPED ACROSS NON - H - 2 AND/OR H-2 BARRIERS

The effect of incompatibility for Mls determinants was studied in lethal graft-versus-host reaction (GVHR) in the mouse. GVHR was induced in adult recipients of the following H-2^k strains: (AKR x B10.BR)F1 (Mls^B/Mls^b); (C3H x B10.BR)F1 (Mls^c/Mls^b); (CBA/J x B10.BR)F1 (Mls^d/Mls^b) and (CBA/H x B10.BR)F1 (Mls^b). Recipient mice were heavily irradiated and grafted with bone marrow and spleen cells from H-2 compatible B10.BR (H-2^k, Mls^b) or H-2 incompatible B10.D2 and B10 donors were normal, while those from B10.BR donors were either normal or pre-immunized against the recipient strains. In all experiments the survival of recipients with Mls^a/Mls^b and Mls^d/Mls^b phenotypes, and only in one experiment of those with Mls^c/Mls^b phenotype was greater and/or the survival time longer than that of recipients expressing only Mls^b. However, late deaths (> 120 days post grafting) observed after grafting of normal B10.BR cells were more frequent in Mls^d/Mls^b than in Mls^b strains. On the other hand, when B10.BR donor cells were pre-immunized against H-2^k compatible (AKR x B10.BR)F1 (Mls^a/Mls^b) or (CBA/J x B10.BR)F1 (Mls^d/Mls^b) strains, the survival time of H-2 incompatible (B10 x B10.BR)F1 (H-2^b/k, Mls^b) recipients was longer than when donor cells were pre-immunized against (CBA/H x B10.BR)F1 (Mls^b) strain. We conclude that donor incompatibility for Mls^a or Mls^d or donor-pre-immunization against Mls^a or Mls^d exerts a protective effect on lethal GVHR developed across non-H-2 or H-2 barriers; the protective effect of Mls^c is less efficient or absent. The Mls-induced protective effect shows the following properties: (a) efficiency in vivo correlates with the capacity of the corresponding alleles to stimulate an in vitro MLR; (b) is efficient in either primary or secondary response to other minor antigens; (c) is not H-2 restricted; (d) is nonspecific; (e) disappears late after grafting; (f) with respect to the genetic background, the early protective effect is followed, late after grafting, by an opposite effect which increases the mortality, suggesting that M/s locus determinants are capable of activating several cell populations with different biological functions.     

Role of vasopressin V2 receptors in modulation of the renal cortico-papillary NaCl gradient

In order to examine if modulation by vasopressin of NaCl transport in Henle's loops (via V2 receptors) can significantly modify medullary ionic hypertonicity, the effects of stimulation or inhibition of these receptors were studied in anaesthetized Wistar rats. Total electrolyte concentration in the medullary interstitium was continuously measured as tissue admittance (reciprocal impedance), using needle electrodes recording from the inner and outer medulla of the in situ kidney. Deamino-[Cys¹,D-Arg⁸]vasopressin (dDAVP], a V2 agonist, infused i.v. at 7.5 ng · min^–1 · kg^–1, significantly increased admittance by 9% and 8% in the inner and outer medulla, respectively. A slightly pressor i.v. infusion of natural arginine vasopressin (AVP) induced pressure natriuresis and did not affect medullary electrolyte concentration. Inhibition of V2 receptors with [d(CH₂)⁵,D-Phe², Ile⁴]-AVP, infused i.v. at 133 g · h^–1 kg^–1 in indomethacin-treated rats, decreased admittance (significant in the inner medulla). Neither of the three agents used caused significant changes in the renal blood flow (RBF) or clearance of inulin (C _in). The demonstration that changing activity of V2 receptors affects the corticopapillary NaCl gradient indicates that, at least in rodents, stimulation of loop salt transport by AVP may represent an additional mechanism enhancing urine concentration.     

Morphology of cycloparaffins crystallized epitaxially on NaCl

The cycloparaffins (CH₂)₃₆ and (CH₂)₆₀ were crystallized epitaxially from solutions on the (001) face of the NaCl crystal at various temperatures. Two types of crystals, so-called edge-on and flat-on crystals, were separately obtained depending on crystallization temperature. The temperature for obtaining edge-on crystals was higher by ca. 10°C than that for flat-on crystals. In both flat-on and edge-on crystals, the long side (b-axis) is aligned to the 〈110〉 direction of NaCl. The (001) plane in the flat-on crystal and (202) in the edge-on crystal are parallel to the substrate surface. The direction of the vector c ′ defined as ? a + c is parallel to the molecular axis in monoclinic cycloparaffin crystals. The angle β′ between c ′ and the a-axis is almost constant at about 119°, while c′ changes linearly with the number of carbon atoms in a molecule. The space group changes from Aa to Ia in the new unit cell with the dimensions a, b, c′ and β′.     

On the molecular weight determination by vapor pressure osmometry (VPO), 2. Molecular weight average obtained by VPO

Provided that in molecular weight determinations by vapor pressure osmometry (VPO) the relationship between M and the measured quantity (δV/c)_c=0 obeys a calibration function of the type (δV/c)_c=0 = KM^?a, the kind of molecular weight average M?_VPO delivered by this method is derived. The deviation of M?_VPO from the true number average molecular weight M?_n is estimated from its dependence on the polydispersity and the exponent a of the calibration function.     

Vasopressin release in response to intracerebroventricular L-alanine and L-arginine, and its dependence upon CSF NaCl concentration

Influences on renal water, electrolyte, and arginine vasopressin (AVP) excretions of 1 h infusions (20 microliters/min) of a neutral (L-alanine) and two basic (L-lysine and L-arginine) amino acids into the lateral cerebral ventricle were studied in hydrated goats, and were compared to effects of control infusions of hypertonic (0.25 M) NaCl. L-alanine (0.11 M) dissolved in hypotonic NaCl caused more pronounced inhibition of the water diuresis and greater increase in AVP excretion than did the control infusions, but, in comparison to the latter, the responses developed very slowly. The effects were further delayed and were much attenuated when L-alanine was administered in isotonic glucose, but became considerably accentuated when isotonic NaCl was used as the solvent. L-lysine (0.09 M) in hypotonic NaCl did not inhibit the water diuresis or cause any apparent AVP release, whereas the corresponding L-arginine infusions caused inhibition of the water diuresis and increase in AVP excretion of approximately the same magnitudes and time courses as the control infusions. Like for L-alanine, these effects became accentuated when L-arginine was dissolved in isotonic NaCl, and became delayed and much attenuated when isotonic glucose was used as the solvent. L-arginine induced a more pronounced increase in renal Na excretion than did L-alanine and 0.25 M NaCl. Since transport together with Na (increasing the Na influx) generally is much more important for cellular uptake of neutral than of basic amino acids, the possibility is discussed that L-alanine here might have caused AVP release by increasing transmembrane Na transport of juxtacerebroventricular Na sensors regulating the AVP secretion--a suggestion supported by the lack of response to the basic L-lysine. The antidiuretic effect of the other basic amino acid, L-arginine, can not be explained along this line. However, with regard to the characteristic differences observed between the responses to L-alanine and L-arginine, the possibility is discussed that the latter might not have acted at a sensory level, but on the final neuronal link in the release of neurohypophyseal hormones, the hypothalamic neurosecretory cells. In contrast to L-alanine and L-arginine, L-lysine appeared to stimulate the appetite of the goats.     

Duration of central action of angiotensin II estimated by its interaction with csf Na+.

In pre-hydrated goats, an urge to drink persisted for approximately half an hour after combined infusions of angiotensin II and hypertonic (0.5 M) NaCl into the lateral or third cerebral ventricle. The intraventricular infusion of angiotensin/glucose solution, having no dipsogenic action of its own, markedly accentuated the dipsogenic and antidiuretic effects of the subsequent intraventricular infusion of hypertonic NaCl. The possibility is discussed that angiotensin may be bound at periventricular receptor sites where it continues to interact with Na+ in eliciting thirst and ADH release for about half an hour.     

Dipsogenic Effects of Intracarotid Infusions of Various Hyperosmolal Solutions

Thirst in response to intracarotid and intravenous infusions (1.5 ml/min) of various hypertonic, equi-osmolal solutions was studied in the goat. Intracarotid infusions of 1 M NaCl and of 2 M fructose induced conspicuous cumulative drinking. The amount of water drunk during intracarotid infusions of 2 M urea and glycerol was only about a third of that consumed during the corresponding infusions of NaCl and fructose. During intracarotid infusions of 2 M galactose and glucose drinking was inconsistent. Of the intravenous infusions only hypertonic NaCl had a consistent dipsogenic effect. However, the amount of water consumed was considerably smaller and the latency time for drinking much longer than during the intracarotid infusions of NaCI. It is concluded that intracarotid infusions of hypertonic solutions act as considerably stronger thirst stimuli than corresponding intravenous infusions, and that the most pronounced dipsogenic effect is obtained by intracarotid infusions of those hypertonic solutions which also most effectively release antidiuretic hormone in the hydrated goat. The possibility is discussed that intracarotid infusions may stimulate the thirst mechanism indirectly via a rise in the Na+ concentration of the cerebrospinal fluid.     

Intrinsic viscosity of intramolecularly crosslinked polyelectrolyte: Poly(vinyl alcohol)/borax systems

The intrisic viscosity [η] of poly(vinyl alcohol) (PVA) was determined in aqueous solutions with various concentrations c_b of borax (Na₂B₄O₇) as functions of molecular weight M and concentration c_s of NaCl as an added salt. Polyelectrolyte viscosity behaviour was observed for the systems containing both borax and NaCl, due to the complexation with negatively charged borate ions B(OH)^?₄ · [η] changes depending on the ionic strength I. It was found that the Stock-mayer-Fixman treatment for the molecular-weight dependence of [η] is valid in the lower molecular-weight range (M < 10⁵), even though the present PVA chain contains some intrachain crosslinks. Theta conditions can be attained at an appropriate concentration c_{s Θ} of NaCl. The value of c_{s Θ} is dependent on c_b, but the conformational parameter from the Stockmayer-Fixman treatment K₀ is almost independent of c_b. The effect of intrachain crosslinks becomes evident only as a considerably large negative value for the excluded volume parameter B at infinite ionic strength. In addition, the electrostatic part of the expansion factor α was found to be linearly correlated to a reduced parameter (M/I)^1/2 for all c_b systems, from the slope of which the charge density was estimated.     

Tolerance to haemorrhage during vasopressin antagonism and/or captopril treatment in conscious sheep

The effect of separate and combined blockade of vasopressin (AVP) V₁-receptors and angiotensin II formation on resistance to a slow venous haemorrhage (0.7 ml kg^-1 min^-1) was studied in six conscious adult sheep by bleeding to the point of an abrupt fall in the mean systemic arterial pressure (MSAP). Intravenous administration of the V₁-receptor antagonist [d(CH₂)₅Tyr(Me)AVP] (10 μg kg^-1) and/or the angiotensin I converting enzyme inhibitor captopril (20 mg+1 mg h^-1) did not cause any significant haemodynamic changes in the normovolaemic animal. The volume of haemorrhage necessary to induce acute hypotension (MSAP < 50 mmHg) was significantly smaller after AVP blockade alone (13.8±0.7 ml kg^-1; P < 0.01) but not after captopril treatment (14.7±1.6 ml kg^-1; n.s.) compared to control animals receiving no drug treatment (16.8±0.6 ml kg^-1). The combined treatment with the AVP antagonist and captopril caused a further decrease in tolerance to haemorrhage (9.4±1.2 ml kg^-1; P < 0.001). Blockade of AVP V₁-receptors was associated with an attenuated increase in systemic vascular resistance immediately after the end of haemorrhage, concomitant with an accentuated lowering of the central venous pressure. In contrast, captopril treatment decreased the degree of vasoconstriction mainly during the second half of the post-haemorrhage observation period of 1 hour. It is concluded that both AVP and angiotensin II contribute to the maintenance of the MSAP during haemorrhage in conscious sheep. During the spontaneous recovery after hypotensive blood loss, a vasoconstrictor effect of AVP is evident mainly during the initial 15 min, whereas at later stages angiotensin II appears to be of relatively greater importance.     

Haupt- und seitenkettenkristallinität bei isotaktischen poly(1-alkylethylen)en, 2. Röntgenographische,kalorimetrische und ramanspektroskopische untersuchungen am it-poly(1-eicosylethylen)

Isotactic poly(1-eicosylethylene) shows three polymorphic modifications. The orthorhombic modification I is formed during melt crystallization at a cooling rate ?<2,5K.s^?1. The dimensions of the unit cell are calculated to be a=0,75 nm, b=8,8 nm and c=0,67 nm. The heat of fusion is 145J.g^?1, the melting point is 363K. The monoclinic modification II is crystallized from the polymer solution (a=0,53 nm, b=10,8 nm, c=0,77 nm, β=94°). The heat of fusion amounts to 120J.g^?1, the melting point is 356K. Modification III is formed during rapid quenching of the melt. The side-chains crystallized closely packed in layers. Modification III shows no main-chain crystallinity. The heat of fusion is 40J.g^?1, the melting point is 348 K. The crystal field splitting in the Raman spectrum of modification +1418/1440cm^?1 indicates an arrangement of the side-chains as in orthorhombic polyethylene with two chains in the subcell. The subcells of both modifications II and III contain only one chain each.